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Introduction: Lung cancer is the leading cause of cancer-associated mortality globally. In particular, non-small cell lung cancer (NSCLC) constitutes the largest percentage of all cases of lung cancer. In clinical practice, radioresistance contributes to poor responses to radiotherapy. Therefore, the demand remains to explore potential novel and effective mechanism underlying radioresistance to improve the efficacy of radiotherapy for NSCLC. Material and methods: Western blotting was conducted to quantify the protein expression of epithelial-mesenchymal transition markers E-cadherin and vimentin in the A549 cell line. The proliferation of A549 cells was measured using the Cell Counting Kit-8 and colony forming assays. In addition, the apoptosis of A549 cells was analyzed by flow cytometry. Invasion and migration by NSCLC cells were quantified using Transwell and wound healing assays. Plasmids were used to overexpress decoy receptor 3 (DcR3) in A549 cells. Xenograft models were established to measure the extent of NSCLC tumor growth in vivo. Results: Our study clarified the activation of the DcR3/protein kinase B (AKT)/glycogen synthase kinase 3β (GSK-3β) pathway in radioresistant NSCLC cells. Oxymatrine (OMT) treatment restored radiosensitivity and inhibited irradiation-induced epithelial-mesenchymal transition (EMT), invasion and migration in NSCLC cells through the DcR3/AKT/GSK-3β pathway in vitro. By contrast, OMT treatment promoted the suppressive effects of radiation on the weight and volume of the xenograft tumors in animal models. Conclusions: OMT suppressed the development of radioresistance in NSCLC cells by promoting radiosensitivity, through the reversal of EMT process by inhibiting the DcR3/AKT/GSK-3β pathway. [ABSTRACT FROM AUTHOR]

Hydroxychloroquine, used initially as an anti-malarial drug, is now recognized for its anti-tumor effects in a range of human cancers. Nevertheless, there has been limited attention given to the molecular mechanisms of anti-tumor action of hydroxychloroquine. Here, we investigated the anti-tumor effect of hydroxychloroquine in human A549 cells and further analyzed the potential molecular mechanisms involved. Hydroxychloroquine was found to effectively inhibit the growth of A549 cells. This inhibition was observed to be both dose-dependent and time-dependent. Moreover, in a tumor xenograft mouse model, hydroxychloroquine remarkably suppressed tumor growth. Mechanistically, treatment with hydroxychloroquine led to the inhibition of phosphorylation in JNK, STAT3 and AKT. This biochemical interference subsequently induced G1 cell cycle arrest and promoted mitochondrial-mediated apoptosis in A549 cells. The findings from this study offered robust evidence supporting the use of hydroxychloroquine as a treatment for nonsmall cell lung cancer (NSCLC). Consequently, hydroxychloroquine emerges as a potential therapeutic agent for the treatment of this cancer. [ABSTRACT FROM AUTHOR]

Background: The objective of this research was to investigate how the combination of semen coicis extract and PD-1 inhibitors can potentially work together to enhance the anti-tumor effects, with a focus on understanding the underlying mechanism. Methods: We obtained the active components and specific targets of semen coicis in the treatment of NSCLC from various databases, namely TCMSP, GeneCard, and OMIM. By utilizing the STRING database and Cytoscape software, we established a protein interaction network (PPI) for the active ingredient of semen coicis and the target genes related to NSCLC. To explore the potential pathways involved, we conducted gene ontology (GO) and biological pathway (KEGG) enrichment analyses, which were further supported by molecular docking technology. Additionally, we conducted cyto-inhibition experiments to verify the inhibitory effects of semen coicis alone or in combination with a PD-1 inhibitor on A549 cells, along with examining the associated pathways. Furthermore, we investigated the synergistic mechanism of these two drugs through cytokine release experiments and the PD-L1 expression study on A549 cells. Results: Semen coicis contains two main active components, Omaine and (S)-4-Nonanolide. Its primary targets include PIK3R1, PIK3CD, PIK3CA, AKT2, and mTOR. Molecular docking experiments confirmed that these ingredients and targets form stable bonds. In vitro experiments showed that semen coicis demonstrates inhibitory effects against A549 cells, and this effect was further enhanced when combined with PD-1 inhibitors. PCR and WB analysis confirmed that the inhibition of the PI3K-AKT-mTOR pathway may contribute to this effect. Additionally, semen coicis was observed to decrease the levels of IFN-γ, IL-6, and TNF-α, promoting the recovery of the human anti-tumor immune response. And semen coicis could inhibit the induced expression of PD‑L1 of A549 cells stimulated by IFN‑γ as well. Conclusion: Semen coicis not only has the ability to kill tumor cells directly but also alleviates the immunosuppression found in the tumor microenvironment. Additionally, it collaboratively enhances the effectiveness of PD-1 inhibitors against tumors by blocking the activation of PI3K-AKT-mTOR. [ABSTRACT FROM AUTHOR]

Fine particulate matter (PM2.5) increases the risks of lung cancer. Epigenetics provides a new toxicology mechanism for the adverse health effects of PM2.5. However, the regulating mechanisms of PM2.5 exposure on candidate gene DNA methylation changes in the development of lung cancer remain unclear. Abnormal expression of the glutathione S transferase (GST) gene is associated with cancer. However, the relationship between PM2.5 and DNA methylation-mediated GST gene expression is not well understood. In this study, we performed GST DNA methylation analysis and GST-related gene expression in human A549 cells exposed to PM2.5 (0, 50, 100 µg/mL, from Taiyuan, China) for 24 h (n = 4). We found that PM2.5 may cause DNA oxidative damage to cells and the elevation of GSTP1 promotes cell resistance to reactive oxygen species (ROS). The Kelch-1ike ECH-associated protein l (Keap1)/nuclear factor NF-E2-related factor 2 (Nrf2) pathway activates the GSTP1. The decrease in the DNA methylation level of the GSTP1 gene enhances GSTP1 expression. GST DNA methylation is associated with reduced levels of 5-methylcytosine (5mC), DNA methyltransferase 1 (DNMT1), and histone deacetylases 3 (HDAC3). The GSTM1 was not sensitive to PM2.5 stimulation. Our findings suggest that PM2.5 activates GSTP1 to defend PM2.5-induced ROS and 8-hydroxy-deoxyguanosine (8-OHdG) formation through the Keap1/Nrf2 signaling pathway and GSTP1 DNA methylation. [ABSTRACT FROM AUTHOR]

Abstract Lung cancer is a major public health issue and heavy burden in China and worldwide due to its high incidence and mortality without effective treatment. It’s imperative to develop new treatments to overcome drug resistance. Natural products from food source, given their wide-ranging and long-term benefits, have been increasingly used in tumor prevention and treatment. This study revealed that Hibiscus manihot L. flower extract (HML) suppressed the proliferation and migration of A549 cells in a dose and time dependent manner and disrupting cell cycle progression. HML markedly enhanced the accumulation of ROS, stimulated the dissipation of mitochondrial membrane potential (MMP) and that facilitated mitophagy through the loss of mitochondrial function. In addition, HML induced apoptosis by activation of the PTEN-P53 pathway and inhibition of ATG5/7-dependent autophagy induced by PINK1-mediated mitophagy in A549 cells. Moreover, HML exert anticancer effects together with 5-FU through synergistic effect. Taken together, HML may serve as a potential tumor prevention and adjuvant treatment for its functional attributes.

Lung cancer is a major public health issue and heavy burden in China and worldwide due to its high incidence and mortality without effective treatment. It's imperative to develop new treatments to overcome drug resistance. Natural products from food source, given their wide-ranging and long-term benefits, have been increasingly used in tumor prevention and treatment. This study revealed that Hibiscus manihot L. flower extract (HML) suppressed the proliferation and migration of A549 cells in a dose and time dependent manner and disrupting cell cycle progression. HML markedly enhanced the accumulation of ROS, stimulated the dissipation of mitochondrial membrane potential (MMP) and that facilitated mitophagy through the loss of mitochondrial function. In addition, HML induced apoptosis by activation of the PTEN-P53 pathway and inhibition of ATG5/7-dependent autophagy induced by PINK1-mediated mitophagy in A549 cells. Moreover, HML exert anticancer effects together with 5-FU through synergistic effect. Taken together, HML may serve as a potential tumor prevention and adjuvant treatment for its functional attributes. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Lung cancer has a high incidence rate worldwide, necessitating the development of new drugs. Although Magnolia figo (Lour.) DC. is known for its medicinal properties, studies on its efficacy against lung cancer are lacking. This study investigated whether the supercritical fluid extract of M. figo (FMO) can induce apoptosis in A549, a human non-small-cell lung cancer cell line. The cell viability was assessed using an MTT assay. A terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) analysis and flow cytometry analysis were conducted. The expression of factors was assessed through Western blotting analyses. Gas chromatography–mass spectrometry (GC-MS) was performed. The results revealed that FMO treatment exhibited cytotoxicity, demonstrating dose-dependent effects. The TUNEL analysis and flow cytometry analysis revealed that FMO induced apoptosis in A549 cells. The Western blotting analysis revealed that FMO upregulated the expression of p53 and Bax protein, and downregulated the expression of Bcl-2 protein. The GC-MS analysis revealed eight components identified in FMO. These findings indicate that FMO can induce A549 apoptosis through the p53/Bcl-2/Bax pathways, confirming the apoptotic effects of M. figo on lung cancer cells. These results highlight the potential, for the first time, of M. figo as a source for developing novel drugs for lung cancer treatment. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

'Globemaster' is an ornamental hybrid cultivar whose parent plants are Allium cristophii and A. macleanii. The chemical constituents of 'Globemaster' bulbs have not yet been examined; thus, a systematic phytochemical investigation was undertaken herein. A series of chromatographic separations of the MeOH extract of 'Globemaster' bulbs afforded 27 steroidal glycosides (1–27), which are classified into 23 spirostanol glycosides (1–8 and 11–25), two furostanol glycosides (9 and 26), a pregnane glycoside (10), and a cholestane glycoside (27). The structures of the hitherto undescribed compounds (1–10) were determined from the two-dimensional NMR spectroscopic data and hydrolysis. The cytotoxicity of the isolated compounds (1–27) toward HL-60 human promyelocytic leukemia cells, A549 human adenocarcinoma lung cancer cells, and SBC-3 human small-cell lung cancer cells was evaluated. Compounds 8, 22, 23, 24, and 26 exhibited cytotoxicity toward all cell lines in a dose-dependent manner, with IC50 values in the 1.3–49 µM range. [ABSTRACT FROM AUTHOR]

Objective The study was conducted to investigate the dephosphorylation of Pseudomonas aeruginosa flagellin (PA FLA) by sweet potato purple acid phosphatase (PAP) and the effect of the enzyme on the flagellin-mediated inflammatory response in the A549 lung epithelial cell line. Methods The activity of sweet potato PAP on PA FLA was assayed at different pH (4, 5.5, 7, and 7.5) and temperature (25°C, 37°C, and 55°C) conditions. The release of interleukin-8 (IL-8) and the activation of nuclear factor kappa- light-chain-enhancer of activated B cells (NF-κB) in A549 cells exposed to PA FLA treated with or without sweet potato PAP was measured using IL-8 and NF-κB ELISA kits, respectively. The activation of toll-like receptor 5 (TLR5) in TLR5-overexpressing HEK-293 cells exposed to PA FLA treated with or without sweet potato PAP was determined by the secreted alkaline phosphatase-based assay. Results The dephosphorylation of PA FLA by sweet potato PAP was favorable at pH 4 and 5.5 and highest at 55°C. PA-FLA treated with the enzyme decreased IL-8 release from A549 cells to about 3.5-fold compared to intact PA FLA at 1,000 ng/mL of substrate. Moreover, PA-FLA dephosphorylated by the enzyme repressed the activation of NF-κB in the cells compared to intact PA FLA. The activation of TLR5 by PA-FLA was highest in TLR-overexpressing HEK293 cells at a substrate concentration of 5,000 ng/mL, whereas PA FLA treated with the enzyme strongly repressed the activation of TLR5. Conclusion Sweet potato PAP has the potential to be a new alternative agent against the increased antibiotic resistance of P. aeruginosa and may be a new conceptual feed additive to control unwanted inflammatory responses caused by bacterial infections in animal husbandry.

In order to develop new anti-cancer drugs more efficiently and reduce side effects based on active drug targets, the virtual drug screening was carried out through the target of G-quadruplexes and 23 hit compounds were, thus, screened out as potential anticancer drugs. Six classical G-quadruplex complexes were introduced as query molecules, and the three-dimensional similarity of molecules was calculated by shape feature similarity (SHAFTS) method so as to reduce the range of potential compounds. Afterwards, the molecular docking technology was utilized to perform the final screening followed by the exploration of the binding between each compound and four different structures of G-quadruplex. In order to verify the anticancer activity of the selected compounds, compounds 1, 6 and 7 were chosen to treat A549 cells in vitro, the lung cancer epithelial cells, for further exploring their anticancer activity. These three compounds were found to be of good characteristics in the treatment of cancer, which revealed the great application prospect of the virtual screening method in developing new drugs. [ABSTRACT FROM AUTHOR]

Scientists are finding the most effective chemotherapeutic agents for the treatment of cancer. In the present study, we evaluated the anticancer mechanism of DPPG, a derivative of DAPG (2,4-diacetylphloroglucinol), for the first time. DPPG and DAPG inhibited 83 and 59% of human colorectal cancer HCT116 cell growth at 40.0 µg/ml, and 74 and 57% of human lung cancer A549 cell growth at 10.0 µg/ml concentrations respectively. Furthermore, DPPG and DAPG inhibited 97 and 73% colony formation of the HCT116 cells at 20.0 µg/ml concentration. DPPG and DAPG induced apoptosis in the HCT116 and A549 cells that was confirmed by Hoechst 33342 and FITC-annexin V staining. This result also revealed that ROS generated in both the HCT116 and A549 cells after treatment with DPPG. However, no ROS production was observed in HCT116 and A549 cells after treatment with DAPG. Both DAPG and DPPG significantly increased the CASP3 protein expression that was detected by staining the cells with the super-view 488-CASP3 substrate. Expression of WNT1 gene was eliminated in DPPG and DAPG treated HCT116. Expression of MAPK1 gene was entirely abolished in DPPG treated cells, whereas a significant decrease was observed for DAPG. An intense band of CASP8 gene product was observed agarose gel for DPPG treated HCT116 cells than DAPG. Molecular docking simulation showed the high binding affinities (≥ 6.5 kcal/mol) of DPPG and DAPG with target proteins WNT1, MAPK1, CASP8, and CASP3 in HCT116 cells. This manuscript demonstrated that DAPG and DPPG inhibited lung and colorectal cancer cells by inducing apoptosis. DAPG and DPPG inhibited A549 and HCT116 cells growth by inducing apoptosis [ABSTRACT FROM AUTHOR]

Copyright of Journal of South-Central Minzu University (Natural Science Edition) is the property of Journal of South-Central Minzu University (Natural Science Edition) Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Half-sandwich iridium(III) (IrIII) anticancer complexes, as promising alternatives to platinum-based drugs, especially for solving resistance to platinum drugs, have demonstrated excellent application prospect. The potency of these IrIII complexes as anticancer agents could be significantly enhanced through the strategic modification of their peripheral ligands. In this study, four structurally varied triphenylamine (TPA)-modified half-sandwich IrIII Schiff base complexes were designed and prepared. The incorporation of TPA unit has effectively endowed these complexes with suitable emission, which facilitates the evaluation of intracellular accumulation and cell morphology. These complexes demonstrated favorable in vitro anti-proliferative activity against A549 cell line (lung cancer cells, derived from alveolar basal epithelial cells), especially for pentamethylcyclopentadiene (Cp*)-based one (IrTS1 and IrTS3), and that is almost 2.5-fold more than cisplatin under the same conditions. Meanwhile, IrTS1 and IrTS3 possessed excellent activity against A549/DDP (cisplatin-resistant) cell line and the similar cytotoxicity to cisplatin against BEAS-2B cell line (derived from the bronchial epithelium of normal human lungs), then following a mitochondria apoptotic channel. Triphenylamine-regulated iridium complexes could lead to the accumulation of reactive oxygen species and show a mitochondrial apoptosis channel for A549 cells. [Display omitted] • TPA-appended half-sandwich iridium complexes showed favorable luminescence. • Complexes had antiproliferative and antimigration activity against A549 cells. • Complexes overcome cisplatin resistance and became a potential alternative. • Complexes target mitochondria and led to A549 cell apoptosis. [ABSTRACT FROM AUTHOR]

Abstract Background Acute respiratory distress syndrome (ARDS) is characterized by refractory hypoxemia caused by accumulation of pulmonary fluid, which is related to inflammatory cell infiltration, impaired tight junction of pulmonary epithelium and impaired Na, K-ATPase function, especially Na, K-ATPase α1 subunit. Up until now, the pathogenic mechanism at the level of protein during lipopolysaccharide- (LPS-) induced ARDS remains unclear. Methods Using an unbiased, discovery and quantitative proteomic approach, we discovered the differentially expressed proteins binding to Na, K-ATPase α1 between LPS-A549 cells and Control-A549 cells. These Na, K-ATPase α1 interacting proteins were screened by co-immunoprecipitation (Co-IP) technology. Among them, some of the differentially expressed proteins with significant performance were identified and quantified by liquid chromatography-tandem mass spectrometry (LC–MS/MS). Data are available via ProteomeXchange with identifier PXD032209. The protein interaction network was constructed by the related Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. Several differentially expressed proteins were validated by Western blot. Results Of identified 1598 proteins, 89 were differentially expressed proteins between LPS-A549 cells and Control-A549 cells. Intriguingly, protein–protein interaction network showed that there were 244 significantly enriched co-expression among 60 proteins in the group control-A549. while the group LPS-A549 showed 43 significant enriched interactions among 29 proteins. The related GO and KEGG analysis found evident phenomena of ubiquitination and deubiquitination, as well as the pathways related to autophagy. Among proteins with rich abundance, there were several intriguing ones, including the deubiquitinase (OTUB1), the tight junction protein zonula occludens-1 (ZO-1), the scaffold protein in CUL4B-RING ubiquitin ligase (CRL4B) complexes (CUL4B) and the autophagy-related protein sequestosome-1 (SQSTM1). Conclusions In conclusion, our proteomic approach revealed targets related to the occurrence and development of ARDS, being the first study to investigate significant differences in Na, K-ATPase α1 interacting proteins between LPS-induced ARDS cell model and control-A549 cell. These proteins may help the clinical diagnosis and facilitate the personalized treatment of ARDS. Graphical Abstract

Background: The endoplasmic reticulum (ER) is a cellular membrane-bound organelle whereby proteins are synthesized, folded and glycosylated. Due to intrinsic (e.g., genetic) and extrinsic (e.g., environmental stressors) perturbations, ER proteostasis can be deregulated within cells which triggers unfolded protein response (UPR) as an adaptive stress response that may impact the migration and invasion properties of cancer cells. However, the mechanisms underlying the nickel compounds on lung cancer cell migration and invasion remain uncertain. Objective: We aimed to study whether Nickel chloride (NiCl2) induces ER stress in lung cancer cells, and whether ER stress is involved in modulating epithelial-mesenchymal transition (EMT) and migration by Smads and MAPKs pathways activation following NiCl2 treatment. Methods: A549 cells were treated with NiCl2 to determine the cell viability using MTT assay. The wound healing assay was used to evaluate cell migration ability. ER ultrastructure was observed by transmission electron microscopy. Western blotting assay was performed to evaluate the protein levels of BIP, PERK, IRE-1α, XBP-1 s, and ATF6 for ER stress and UPR, E-cadherin and Vimentin for EMT, p-Smad2/3, p-ERK, p-JNK, and p-P38 for activation of Smads and MAPKs signaling pathways. Results: The expression levels of BIP, PERK, IRE-1α, XBP-1 s, and ATF6 were significantly increased following treatment with NiCl2 in time- and dose-effect relationship. The ER stress inhibitor 4-PBA downregulated the expression levels of the above five proteins, and reversed the decrease in E-cadherin protein level and the increase in vimentin protein expression and cell migration abilities caused by NiCl2. Furthermore, 4-PBA significantly reduced nickel chloride-induced Smad2/3 and p38 MAPK pathway activation, while not affected ERK and JNK MAPK pathways. Conclusion: NiCl2 triggers ER stress and UPR in A549 cells. Moreover, 4-PBA alleviates NiCl2-induced EMT and migration ability of A549 cells possibly through the Smad2/3 and p38 MAPK pathways activation, rather than ERK and JNK MAPK pathways.

Delphinidin (Del) is an anthocyanin component with high in vitro antioxidant capacity. In this study, based on the screening of a cell model, gas chromatography-time of flight mass spectrometry (GC-TOF/MS) was used to evaluate the effect of Del pre-protection on the metabolite levels of intracellular oxidative stress induced by paraquat (PQ). According to the cytotoxicity and reactive oxygen species (ROS) responses of four lung cell lines to PQ induction, A549 cell was selected and treated with 100 μM PQ for 12 h to develop a cellular oxidative stress model. Compared with the PQ-induced group, the principal components of the Del pretreatment group had significant differences, but not significant with the control group, indicating that the antioxidant activity of Del can be correlated to the maintenance of metabolite levels. Del preconditioning protects lipid-related metabolic pathways from the disturbance induced by PQ. In addition, the levels of amino acid- and energy-related metabolites were significantly recovered. Del may also exert an antioxidant effect by regulating glucose metabolism. The optimal combinations of biomarkers in the PQ-treatment group and Del-pretreatment group were alanine-valine-urea and alanine-galactose-glucose. Cell metabolome data provided characteristic fingerprints associated with the antioxidant activity of Del. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effect of cystathionine β-synthase (CBS) on the proliferation of lung adenocarcinoma A549 cells through the AKT/cyclin D1 pathway and its molecular mechanism. Methods: Expression of CBS and AKT/cyclinD1-related proteins in lung adenocarcinoma tissues was analyzed by cBioPortal database. The CBS expression in collected lung adenocarcinoma tissues from Chinese patients was verified by immunofluorescence method. WB assay was performed to detect the expression of cysteine metabolism and AKT/cyclin D1 pathway-related proteins in A549 cells and their transplanted tumors, and CBS DNA methylation sequencing was performed to detect the effect of its methylation on CBS mRNA expression in lung cancer cells. The pCW57.1-myrAKT plasmid was co-transfected with RNA interference control plasmid pGIPZ-CBS-nc-shRNA, interference plasmid pGIPZ-CBS-shNRA1 and pGIPZ-CBS-shNRA2, respectively, into A549 cells, which were further sub-divided into DOX+ and DOX- groups. The colony formation ability of A549 cells in each group after transfection was examined by cell colony formation assay. The effect of overexpression of CBS on the growth of transplanted tumors was examined by CBSwtA549 cell- and CBSI278TA549 celltransplanted tumor assay, and AzMC fluorescence staining and immunohistochemistry were used to detect H2S levels and Ki-67 positivity in transplanted tumor tissues, respectively. Results: Both database analysis and tissue specimens showed that CBS was lowly expressed in lung adenocarcinoma tissues compared with para-cancerous tissues (all P<0.01); CBS protein was lowly expressed in A549, SKMES1 and NCIH460 cells compared with SV-40 cells (all P<0.01), while p-AKT and cyclin D1 protein levels were highly expressed (all P<0.01). Overexpression of AKT in A549 cells significantly promoted the formation of cell colonies (P<0.01), and knockdown of CBS on this basis further promoted the formation of cell colonies (all P<0.01). Transplantation tumor experiments showed that CBS, RB and P21 protein expression was elevated, H2S level was increased, tumor volume was decreased and Ki-67 positivity was reduced in the DOX+ CBSWT group compared with those in the DOX- CBSWT group (all P<0.01); CBS expression was elevated in the DOX+ CBSI278T group compared with the DOX-CBSI278T group (P<0.01), but the changes in H2S level and transplantation tumor volume were not significant. Conclusions: CBS is lowly expressed in lung adenocarcinoma tissues and A549 cells, while the AKT/cyclinD1 pathway is activated. Overexpression or knockdown of CBS can inhibit or promote the growth of A549 cells and their transplanted tumors, and CBS and AKT/cyclin D1 pathway-related proteins may be the potential targets and markers for lung adenocarcinoma. [ABSTRACT FROM AUTHOR]

Lung cancer is one of the most common malignant tumors, with the highest mortality rate in the world, and its incidence is second only to breast cancer. It has posed a serious threat to human health. Cisplatin, a metal-based drug, is one of the most widely used chemotherapeutic agents for the treatment of various cancers. However, its clinical efficacy is seriously limited by numerous side effects and drug resistance. This has led to the exploration and development of other transition metal complexes for the treatment of malignant tumors. In recent years, iridium-based complexes have attracted extensive attention due to their potent anticancer activities, limited side effects, unique antitumor mechanisms, and rich optical properties, and are expected to be potential antitumor drugs. In this review, we summarize the recent progress of iridium complexes against lung cancer and introduce their anti-tumor mechanisms, including apoptosis, cycle arrest, inhibition of lung cancer cell migration, induction of immunogenic cell death, etc. [ABSTRACT FROM AUTHOR]

Exosomes participate in intercellular communication by shuttling various small molecules from donor to recipient cells. We aimed to examine the role of exosomes and exosomal miRNAs in influenza virus infection. The results showed that influenza A/H1N1pdm09 infection could promote A549 cells to secrete exosomes, while blocking the generation of exosomes reduced viral RNA production. A total of 97 exosomal miRNAs with significantly altered expression were identified during influenza infection. Of 12 candidate miRNAs chosen for further validation, ten were confirmed by qRT-PCR. Among 5978 predicted target genes，we found 37 interferon pathway-related genes to be the potential targets of 29 differentially expressed miRNAs. Many target genes were annotated to various KEGG signaling pathways, some of which played important roles in influenza infection. These data will help to further understand the mechanism of influenza virus-host interactions, which is important for the development of preventative and therapeutic strategies against influenza virus. • Influenza A/H1N1pdm09 infection promotes A549 cells to secrete exosomes. • Blocking the generation of exosomes reduced viral RNA production. • A group of exosomal miRNAs are differentially expressed during influenza A/H1N1pdm09 infection. • The predicted targets of differentially expressed miRNAs are involved in various pathways important for influenza infection. [ABSTRACT FROM AUTHOR]

Presented here is a straightforward detection system designed to track non-small cell lung cancer (specifically A549 cells) using a combination of liquid crystals (LCs) and aptamer sequences, marking a pioneering approach in this field. A change in the alignment of LCs from perpendicular to random status by the aptamer-cell complex altered the murky polarized background of the aptasensor to multicolored. The LC-designed aptasensor could determine A549 cancerous cells in the range of 2.0E+01−7.0E+07 cell mL−1 with a limit of detection (LOD) as low as 10 cell mL−1. Through precise quantification of A549 cells in human serum samples diluted 20 times, with recovery rates ranging from 97.59 % to 101.31 %, the suggested aptasensor proves to be a dependable method for cancer screening. Furthermore, the LC aptasensor was identified as a fast sensing array due to a 10-min incubation period for the aptamer-cell complexation. The LC aptasensor is label-free, operator-independent, low-cost, sensitive, and user-friendly, making it potent as a miniaturized portable sensing chip for efficient healthcare monitoring. [Display omitted] • An LC-based aptasensor was developed for monitoring A549 cancerous cells for the first time. • The sensing was based on the change in alignment of LCs by the aptamer-target interaction. • A549 cells could be detected with an ultra-low detection limit of 10 cell mL−1. • The aptasensor could successfully monitor A549 cells in the human serum samples. [ABSTRACT FROM AUTHOR]

Cell surface receptors play a key role in intracellular signaling, and their overexpression and activation are among the drivers of multiple diseases. Selective inhibition of cell surface receptors is important for regulating intracellular signaling pathways and cell behavior. Here, we design engineered aptamers to selectively inhibit receptor function. In this strategy, the aptamer specifically recognizing the extracellular structural domain of the EGFR, was conjugated to an adamantane moiety through linking arms of various lengths in order to obtain better performances toward EGFR. These interactions inhibit EGFR dimerization, thereby impeding the activation of downstream signaling pathways. It is shown that the adamantane-modified aptamers exhibit superior inhibition of downstream effector proteins relative to the unmodified aptamers. The optimal inhibitory effect was observed with a linker arm of 40 T-base in length. Notably, the best-performing adamantane-modified aptamer specifically binds to A549 cells with a dissociation constant (22.6 ± 4.5 nM) that is approximately 4-fold lower than that of the parent EGFR aptamer (94.4 ± 21.9 nM). We further combine the use of the adamantane-modified aptamer with that of genistein, a natural isoflavone compound with EGFR tyrosine kinase inhibition activity, to enhance the inhibitory effect on EGFR and its downstream signaling employing a synergistic action. This study is expected to provide a versatile approach for the improvement of existing aptamers obtaining increased selective inhibition of cell surface receptors. [ABSTRACT FROM AUTHOR]

Background: Acute respiratory distress syndrome (ARDS) is characterized by refractory hypoxemia caused by accumulation of pulmonary fluid, which is related to inflammatory cell infiltration, impaired tight junction of pulmonary epithelium and impaired Na, K-ATPase function, especially Na, K-ATPase α1 subunit. Up until now, the pathogenic mechanism at the level of protein during lipopolysaccharide- (LPS-) induced ARDS remains unclear. Methods: Using an unbiased, discovery and quantitative proteomic approach, we discovered the differentially expressed proteins binding to Na, K-ATPase α1 between LPS-A549 cells and Control-A549 cells. These Na, K-ATPase α1 interacting proteins were screened by co-immunoprecipitation (Co-IP) technology. Among them, some of the differentially expressed proteins with significant performance were identified and quantified by liquid chromatography-tandem mass spectrometry (LC–MS/MS). Data are available via ProteomeXchange with identifier PXD032209. The protein interaction network was constructed by the related Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. Several differentially expressed proteins were validated by Western blot. Results: Of identified 1598 proteins, 89 were differentially expressed proteins between LPS-A549 cells and Control-A549 cells. Intriguingly, protein–protein interaction network showed that there were 244 significantly enriched co-expression among 60 proteins in the group control-A549. while the group LPS-A549 showed 43 significant enriched interactions among 29 proteins. The related GO and KEGG analysis found evident phenomena of ubiquitination and deubiquitination, as well as the pathways related to autophagy. Among proteins with rich abundance, there were several intriguing ones, including the deubiquitinase (OTUB1), the tight junction protein zonula occludens-1 (ZO-1), the scaffold protein in CUL4B-RING ubiquitin ligase (CRL4B) complexes (CUL4B) and the autophagy-related protein sequestosome-1 (SQSTM1). Conclusions: In conclusion, our proteomic approach revealed targets related to the occurrence and development of ARDS, being the first study to investigate significant differences in Na, K-ATPase α1 interacting proteins between LPS-induced ARDS cell model and control-A549 cell. These proteins may help the clinical diagnosis and facilitate the personalized treatment of ARDS. [ABSTRACT FROM AUTHOR]

With the development of precision medicine, antigen/antibody-targeted therapy has brought great hope to tumor patients; however, the migration of tumor cells, especially a small number of cells flowing into blood or other tissues, remains a clinical challenge. In particular, it is difficult to use functional gold nanomaterials for targeted clinical tumor diagnosis while simultaneously obtaining stable and highly sensitive Raman signals. Therefore, we developed a detection method for functional Au Nanostars (AuNSs) with dual signal enhancement that can specifically track location and obtain high-intensity surface-enhanced Raman scattering (SERS) signals. First, AuNSs with specific optical properties were synthesized and functionalized. The Raman dye 4-mercapto-hydroxybenzoic acid and polyethylene glycol were coupled with the tumor marker, epidermal growth factor receptor, to obtain the targeted SERS probes. In addition, a detection chip was prepared for Raman detection with physical enhancement, exhibiting a 40-times higher signal intensity than that of quartz glass. This study combines physical enhancement and SERS enhancement technologies to achieve dual enhancement, enabling the detection of a highly sensitive and stable Raman signal; this has potential clinical value for antigen/antibody-targeted tumor diagnosis and treatment. [ABSTRACT FROM AUTHOR]

A diesel exhaust particle (DEP) is a type of particulate matter that is easily produced from combustion in a diesel power engine. It has been reported that DEPs can cause short- and long-term health problems. This is because DEPs are complex mixtures that are highly inhalable through the airways due to their small particle size. However, the relationship between intracellular localization of DEPs after their deposition in the lungs and the subsequent biological responses remains to be clarified. This is due to difficulties in distinguishing particles that are inside the cells from those that are outside. In this study, A549 human lung epithelial cells were exposed to DEPs at concentrations of 0, 25, 75, or 200 µg/mL for different periods, after that particles in the A549 cells were analyzed by three-dimensional (3D) images obtained from a Raman microscope. The cytotoxic effects of DEPs on the A549 cells were investigated by measuring cell viability, the levels of intracellular reactive oxygen species (ROS) and cell death. The Raman microscopy revealed that the particles invaded the A549 cells, and at a concentration of 200 µg/mL, they markedly decreased cell viability, increased intracellular ROS production, triggered late apoptosis/necrosis and induced nuclear damage. These results suggest that intracellular DEPs exposed at a high concentration may be highly toxic and can impair the viability of A549 cells. Furthermore, the 3D images from the Raman microscopy can be used to evaluate intracellular particle dynamics. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Kaempferia galanga L. belongs to the family of Zingiberaceae, an endangered medicinal plant with pharmacology activities. Ethyl-p-methoxycinnamate (EPMC) is an essential phytoconstituent of K. galanga rhizomes. Several studies have reported that EPMC has anticancer activities in several cancer cells, including CL-6 gallbladder cancer cells, HepG2liver cancer cells, MCF-7 breast cancer cells, and Raji lymphoma cancer cells. However, studies on A549 lung cancer and B16 melanoma cancer cells have not been reported. This study aimed to determine the anticancer activity of EPMC against A549 lung cancer and B16 melanoma cancer cells. EPMC was obtained by extraction using n-hexane, then recrystallized with chloroform. The isolate was then analyzed by thin-layer chromatography (TLC), and the structure was characterized by Fourier Transform Infrared (FTIR) and Nuclear Magnetic Resonance (NMR) spectroscopy. Cytotoxic activity was determined under Presto Blue assay. Based on the result, EPMC from K. galanga showed the cytotoxic effect on B16 cells with an IC50 value of 97.09 μg/mL, whereas EPMC showed no significant cytotoxic effect on A549 with an IC50 value of 1407.75 μg/mL. It was concluded that EPMC has potential cytotoxic on B16 melanoma cancer cells, but it showed inactive activity against A549 lung cancer cells. Further molecular mechanism underlying EPMC cytotoxic activity needs to be conducted.

Tumor metastasis and invasion are the main impediments to lung adenocarcinoma successful treatment. Previous studies demonstrate that chemotherapeutic agents can elevate the malignancy of cancer cells other than their therapeutic effects. In this study, the effects of transient low-dose cisplatin treatment on the malignant development of lung adenocarcinoma cells (A549) were detected, and the underlying epigenetic mechanisms were investigated. The findings showed that A549 cells exhibited epithelial-mesenchymal transition (EMT)-like phenotype along with malignant progression under the transient low-dose cisplatin treatment. Meanwhile, low-dose cisplatin was found to induce contactin-1 (CNTN-1) upregulation in A549 cells. Subsequently, we found that further overexpressing CNTN-1 in A549 cells obviously activated the EMT process in vitro and in vivo, and caused malignant development of A549 cells in vitro. Taken together, we conclude that low-dose cisplatin can activate the EMT process and resulting malignant progression through upregulating CNTN-1 in A549 cells. The findings provided new evidence that a low concentration of chemotherapeutic agents could facilitate the malignancy of carcinoma cells via activating the EMT process other than their therapeutic effects. [ABSTRACT FROM AUTHOR]

Objective To investigate the role of autophagy in hypoxia-activated CaSR(calcium-sensing receptor,CaSR) in mediating migration of A549 cells. Methods A549 cells in the logarithmic growth phase were randomly divided into control group(N), hypoxia group (H), hypoxia agonist group (H+Gd), hypoxia inhibitor group (H+NPS), and autophagy pathway inhibitor group (H+Gd+3-MA).Western blot was used to detect the expression of CaSR and autophagy protein (Beclin-1) in the cells; Cell scratch experiment was used to detect migration of A549 cells; Transwell assay was applied to evaluate the invasion of A549 cells. Results Hypoxia resulted in increased CaSR expression in A549 cells (P＜0.05), a decreased expression of autophagic effector protein Beclin-1(P＜0.05), increased the percentage of cell healing per unit time (P＜0.05), and the number of cell invasion-permeable membranes (P＜0.05).GdCl3 strengthened the effect of hypoxia, while NPS2390 did weaken the effect of hypoxia. On the basis of hypoxia and GdCl3 conditions, 3-MA further increased the expression of metastasis related indicators of A549 cells, but not the autophagy related indicators. Conclusions CaSR activation promotes migration and invasion of A549 cells by down-regulating autophagy.

Fine particulate matter (PM2.5) is detrimental to the human respiratory system. However, the toxicity of PM2.5 and its associated potentially harmful species, notably novel pollutants like environmentally persistent free radicals (EPFRs), remains unclear. Therefore, one-year site monitoring and ambient air PM2.5 sampling in the Nanjing urban area was designed to investigate the relationships between chemical compositions (carbon fractions, metallic elements, and water-soluble ions) and EPFRs, and change in cytotoxicity with varying PM2.5 components. Oxidative stress (reactive oxygen species, ROS), inflammatory injury (IL-6 and TNF-α), and membrane injury (LDH) of human lung epithelial cells (A549) induced by PM2.5 were analyzed using in vitro cytotoxicity test. Both the composition and toxicity of PM2.5 from different seasons were compared. The average daily exposure of urban PM2.5 associated EPFRs load in Nanjing were 2.29 × 1011 spin m−3. Their exposure concentration and cytotoxic damage ability were stronger in the cold season than warm. The particle compositions of metals and carbon fractions were significantly positively correlated with EPFRs. The airborne EPFRs, organic carbon (OC), and heavy metal Cu, As, and Pb may pose principal cell damage ability, which is worthy of further study interlinking aerosol pollution and health risks.

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Sepsis, with its high morbidity and mortality, is a difficult problem in critical care medicine. The purpose of this study is to investigate the involvement of GRB2‐associated binding protein 1 (GAB1) in septic lung injury. Lipopolysaccharide (LPS)‐induced mouse model and A549 cell model were used to simulate septic lung injury. Haematoxylin and eosin (H&E) staining was used to observe the pathological changes. The terminal‐deoxynucleotidyl transferase/(TdT)‐mediated dUTP‐biotin nick end labelling (TUNEL) staining and flow cytometry were used to detect apoptosis. The levels of inflammatory factors in the bronchoalveolar lavage fluid (BALF) were determined by enzyme‐linked immunosorbent assay (ELISA). In LPS‐induced sepsis mice, GAB1 expression was markedly reduced, and GAB1 overexpression significantly attenuated cell apoptosis and decreased levels of macrophages, neutrophils, and inflammatory factors in the BALF. Our results also demonstrated that GAB1 overexpression significantly reduced LPS‐induced apoptosis and inflammation of A549 cells. More importantly, GAB1 overexpression significantly inhibited the Toll‐like receptor/ NFkappaB (TLR4/NF‐κB) pathway, while silencing GAB1 significantly activated the TLR4/NF‐κB pathway and induced apoptosis and increased expression of inflammatory factors. However, the TLR4 inhibitor TAK‐242 eliminated the effect of GAB1 silencing on A549. In conclusion, GAB1 is a key regulator of sepsis by inhibiting TLR4/NF‐κB mediated apoptosis and inflammation. [ABSTRACT FROM AUTHOR]

Inorganic photocatalysts have been regarded as a promising candidate in the domain of tumor photodynamic therapy (PDT) due to their inspirational photocatalytic activity. In this study, a Bi4O5Br2 photocatalyst was synthesized and it exhibited effective photo-killing activity of A549 cells (a human lung carcinoma epithelial cell line) in vitro. On this basis, we modified Bi4O5Br2 with carbon quantum dots (CQDs) via a hydrolysis method at room temperature, which resulted in an improved photo-killing effect of Bi4O5Br2 to A549 cells. The samples and the interaction between samples and cells were fully characterized. It has been found that the loading of CQDs on Bi4O5Br2 can reduce the hydration ratio, increase the cellular uptake and improve the photogenerated reactive oxygen species (ROS) as compared with pristine Bi4O5Br2. Electron spin resonance (ESR) analysis and radical-trapping experiments manifested that the ROS contributed to PDT may be ·O2− and ·OH. This study may provide a useful strategy to ameliorate the penetrability, cell compatibility and PDT effect upon cancer cells of other inorganic photocatalysts. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Chinese Institute of Food Science & Technology / Zhongguo Shipin Xuebao is the property of Journal of Chinese Institute of Food Science & Technology Periodical Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The aim of this work is to apply Solutol® HS15 and TPGS to prepare self-assembled micelles loading with ginsenoside Rh2 to increase the solubility of ginsenoside Rh2, hence, improving the antitumor efficacy. Ginsenoside Rh2-mixed micelles (Rh2-M) were prepared by thin film dispersion method. The optimal Rh2-M was characterized by particle size, morphology, and drug encapsulation efficiency. The enhancement of in vivo anti-tumor efficacy of Rh2-M was evaluated by nude mice bearing tumor model. The solubility of Rh2 in self-assembled micelles was increased approximately 150-folds compared to free Rh2. In vitro results demonstrated that the particle size of Rh2-M is 74.72 ± 2.63 nm(PDI = 0.147 ± 0.15), and the morphology of Rh2-M is spherical or spheroid, and the EE% and LE% are 95.27 ± 1.26% and 7.68 ± 1.34%, respectively. The results of in vitro cell uptake and in vivo imaging showed that Rh2-M could not only increase the cell uptake of drugs, but also transport drug to tumor sites, prolonging the retention time. In vitro cytotoxicity and in vivo antitumor results showed that the anti-tumor effect of Rh2 can be effectively improved by Rh2-M. Therefore, Solutol® HS15 and TPGS could be used to entrapping Rh2 into micelles, enhancing solubility and antitumor efficacy.

Background Despite the medical uses of lidocaine has been well-characterized, the study of lidocaine’s pharmacological function other the anaesthetic effect was never stopped. This study designed to reveal the effect of lidocaine on the growth and metastasis of lung cancer in vitro.Methods A549 and NCI-H1299 cells were treated by lidocaine for 24 h. miR-539 expression in cell was silenced by transfection with the specific inhibitor. The changes in cell growth and metastasis were determined using CCK-8 assay and western blot. Luciferase activity assay was performed to assay if EGFR was a target of miR-539. Western blot was used to test the activation of EGFR downstream signalling.Results Lidocaine suppressed the viability, migration, and invasion of A549 and NCI-H1299 cells while induced apoptotic death. Lidocaine elevated the expression of miR-539. The anti-tumour properties of lidocaine towards A549 and NCI-H1299 cells were partially attenuated when miR-539 was silenced. EGFR was a target of miR-539. Lidocaine repressed the activation of ERK and PI3K/AKT pathways also via regulating miR-539.Conclusion The anti-growth and anti-metastatic effects of lidocaine towards lung cancer cells. The anti-tumour properties of lidocaine may be partial via up-regulation of miR-539, which blocked EGFR signalling by directly binding with EGFR.

Delphinidin (Del) is an anthocyanin component with high in vitro antioxidant capacity. In this study, based on the screening of a cell model, gas chromatography-time of flight mass spectrometry (GC-TOF/MS) was used to evaluate the effect of Del pre-protection on the metabolite levels of intracellular oxidative stress induced by paraquat (PQ). According to the cytotoxicity and reactive oxygen species (ROS) responses of four lung cell lines to PQ induction, A549 cell was selected and treated with 100 μM PQ for 12 h to develop a cellular oxidative stress model. Compared with the PQ-induced group, the principal components of the Del pretreatment group had significant differences, but not significant with the control group, indicating that the antioxidant activity of Del can be correlated to the maintenance of metabolite levels. Del preconditioning protects lipid-related metabolic pathways from the disturbance induced by PQ. In addition, the levels of amino acid- and energy-related metabolites were significantly recovered. Del may also exert an antioxidant effect by regulating glucose metabolism. The optimal combinations of biomarkers in the PQ-treatment group and Del-pretreatment group were alanine-valine-urea and alanine-galactose-glucose. Cell metabolome data provided characteristic fingerprints associated with the antioxidant activity of Del.

Objective: To investigate the effect of lncRNA MAFG antisense RNA1 (lncRNA MAFG-AS1) regulating miR-532-3p on the glycolysis of lung cancer A549 cells. Methods: The expression levels of MAFG-AS1 and miR-532-3p in human lung cancer A549 cells and normal lung epithelial BEAS-2B cells were detected by qPCR. A549 cells with MAFG-AS1 downregulation or miR-532-3p overexpression were constructed by liposome transfection technique, respectively. The glucose consumption and lactate secretion in cell culture supernatant of A549 cells were detected by visible spectrophotometry, and the mRNA and protein expression levels of pyruvate kinase M2 (PKM2) and hexokinase 2 (HK2) in A549 cells were detected using qPCR and WB, respectively. The targeting relationship between MAFG-AS1 and miR-532-3p was verified by Dual luciferase reporter gene assay, and the effects of co-downregulation of MAFG-AS1 and miR-532-3p on glucose uptake, lactate secretion and expression of PKM2 and HK2 in A549 cells were observed. Results: Compared with BEAS-2B cells, the expression of MAFG-AS1 was upregulated while miR-532-3p expression was downregulated in A549 cells (all P<0.01). Glucose consumption, lactate secretion and the protein and mRNA expressions of PKM2 and HK2 were inhibited by MAFG-AS1 downregulation or miR-532-3p overexpression (all P<0.01). miR-532-3p could bind to MAFG-AS1 and inhibit the luciferase activity of wild-type MAFG-AS1 cells (P<0.01). Downregulation of MAFG-AS1 could increase the expression of miR-532-3p (P<0.01), while the co-downregulation of miR-532-3p could reverse the effect of MAFG-AS1 downregulation on glucose uptake, lactate secretion and the expression of PKM2 and HK2 in A549 cells (all P<0.01). Conclusion: Downregulation of MAFG-AS1 can inhibit the glycolysis of A549 cells by promoting the expression of miR-532-3p. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Lung cancer is the most common malignant tumor and is the leading cause of cancer-related deaths worldwide. Extraction of bioactive substances from herbs is considered as an alternative method to traditional treatment. 6-Gingerol is a naturally occurring phenol found in ginger that can be used to treat tumors and suppress inflammation. To determine whether 6-Gingerol can be used as a therapeutic agent for tumors. In this study, tumor-bearing mice were used as an animal model and A549 as a cell model. Western blot was used to detect the expression of autophagy related proteins ubiquitin-specific peptidase 14 (USP14), Beclin1, microtubule-associated protein light chain 3 (LC3) and ferroptosis related proteins nuclear receptor coactivator 4 (NCOA4), ferritin heavy chain 1 (FTH1), transferrin receptor 1 (TfR1), glutathione peroxidase 4 (GPX4), activating transcription factor4 (ATF4) in vivo and in vitro. MTT and EdU were used to detect the viability of A549 cells. H&E and immunofluorescence were used to localize and detect the expression of proteins. The detection of reactive oxygen species was performed using fluorescence probes. It was found that the administration of 6-Gingerol decreased the expression of USP14, greatly increased the number of autophagosomes, reactive oxygen species (ROS) and iron concentration, decreased the survival and proliferation rate of A549 cells, and significantly decreased tumor volume and weight. The results indicate that 6-Gingerol inhibits lung cancer cell growth via suppression of USP14 expression and its downstream regulation of autophagy-dependent ferroptosis, revealing the function and efficacy of 6-Gingerol as a therapeutic compound in A549 and its possible mechanism of action.

Objectives: Physalis peruviana L. is a medicinal herb and its consumption increases annually in The Middle East, also the scientific research on it increases due to its valuable nutrient. Materials and Methods: Methanolic extracts of P. peruviana L. seeds and juice were screened for their anticancer and antioxidant. Gas chromatography-mass spectroscopy profiling was performed for all extracts.. Results: The identification of seeds and juice methanolic extract showed the main sex compounds; ethanol, 2,2'-oxybis-, caffeic acid in both of the extracts. Octadecadienoate ethyl and octadecenoic acid have been found in seed extract, and octadecadienoic acid and ferulic acid were in juice extract. Seeds extract has phenolic and flavonoid content as 53.58 and 45.56, respectively, comparing to juice extract (26.58 and 7.30, respectively). The antioxidant activities of seeds extract using 2,2-diphenyl-1-picrylhydrazyl (DPPH) and ferric reducing antioxidant potential (FRAP) (28.73 at 50 μg/ml and 1164.10, respectively) comparing to juice extract values (4.06 at μg/ml and 848.43, respectively). Conclusion: The conspicuous optimistic result is that seeds extract showed cancer inhibition against human HepG2 and A549 (81.45 and 85.34, respectively) comparing to juice extract (44.06 and 32.06, respectively). Therefore, the demand to increase the usage of Physalis or golden berry in people's diet is a demand to face the environmental oxidative stress. [ABSTRACT FROM AUTHOR]