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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.)

Background: Epithelial ovarian cancer (EOC) is the most common type of ovarian cancer. About 90% of ovary tumors are epithelial. The current treatment for EOC involves surgical debulking of the tumors followed by a combination of chemotherapy. While most patients achieve complete remission, many EOCs will recur and develop chemoresistance. The cancer cells can adapt to several stress stimuli, becoming resistant. Therefore, new ways to fight resistant cells during the disease are being studied. Recently, exosomes, which reflect cell behavior in normal and pathological conditions such as epithelial ovarian cancer, are of academic interest as new biomarkers for diagnosis and therapy. Consequently, the current study aimed to investigate the research output of exosomes in EOC. Method: A bibliometric method was used for analyzing publications on exosome and epithelial ovarian cancer from the beginning to 15 October 2022 by searching keywords in Scopus, PubMed and Google scholar. Annual scientific publications, authors, citations, journals, co-authorships, and keywords co-occurrence were analyzed and plotted using Microsoft Office Excel and VOS viewer. 39 original journal articles and 3 reviews have been published since 2015 up to 15 October 2022. Results: The findings showed that China is the top country in research output, international collaborations, organization, author, and sponsorship. The top journals were the Journal of Ovarian Research, Oncotarget, and Tumor Biology, all in the United States. The top institution was Shanghai Jiao Tong University in China. The top author was Xipeng Wang. Co-occurrence analysis showed that academics' interest is toward:1) 1) Exosomes as prognostic biomarkers of EOC as well as their role in the proliferation and migration of cells. 2) The role of exosomes in metastasis through different mechanisms; 3) The role of exosomes in epithelial-mesenchymal transition of ovarian cancer cells; 4) The diagnostic role of EVs in EOC; and 5) Conferring chemoresistance in EOC through the exosomal transfer of miRNAs. Conclusion: Research on the exosome and EOC has an increasing trend, and China is much more involved than other countries in research, financial support, and international cooperation. These findings could aid researcher in understanding novel ideas and subjects interested by sponsors in this field. [ABSTRACT FROM AUTHOR]

The incidence of major depressive disorder (MDD) is increasing all over the world. There is a great need for complementary or alternative therapies with high safety, few side effects, and precise efficacy to care for MDD. In China, acupuncture has significant laboratory data and clinical trials to demonstrate its antidepressant efficacy. However, there is no clear answer as to how it works. Exosomes are membranous vesicles that rely on cellular multivesicular bodies (MVBs) fused to the cell membrane for release into the extracellular matrix. Almost all cell types are capable of producing and releasing exosomes. As a result, exosomes contain complex RNAs and proteins from their relatives (Cells that secretes exosomes). They can cross biological barriers and participate in biological activities, such as cell migration, angiogenesis, and immune regulation. These properties have made them a popular research topic. Some experts have suggested that exosomes may serve as delivery vehicles for acupuncture to work. This presents both an opportunity and a new challenge for improving the protocols of acupuncture as a treatment for MDD. To better define the relationship between MDD, exosomes, and acupuncture, we reviewed the literature from the last few years. Inclusion criteria included randomized controlled trials and basic trials evaluating acupuncture in the treatment or prevention of MDD, the role of exosomes in the development and progression of MDD, and the role of exosomes in acupuncture. We believe that acupuncture may affect the distribution of exosomes in vivo, and exosomes may be a new carrier for acupuncture treatment of MDD in the future. [ABSTRACT FROM AUTHOR]

Polygoni Cuspidati Rhizoma et Radix (syn. rhizomes of Reynoutria japonica Houtt.) is a pharmacopoeial raw material in Europe and China. In traditional medicine, one of the applications for Reynoutria japonica rhizomes is wound healing. In a recent in vitro study, we demonstrated that ethanol and acetone extracts from this herbal drug have the potential to heal oral gum wounds. However, considering that a majority of herbal medicines have been traditionally administered as water decoctions, in the present study, a decoction of Reynoutria japonica rhizomes was prepared and detailed tests to determine its in vitro gingival wound healing activity were conducted. We used the primary human gingival fibroblasts (HGF) incubated with a decoction to determine cell viability (MTT assay), cell proliferation (the confocal laser scanning microscope—CLSM), and cell migration (wound healing assay). Moreover, the collagen type III expression was examined using immunocytochemical staining. The studied decoction was qualitatively and quantitatively characterized using the validated HPLC/DAD/ESI-HR-QTOF-MS method. The Folin–Ciocalteu assay was used to determine the total phenols and tannins content. Additionally, HPLC-RI analysis of decoction and the previously obtained ethanol and acetone extracts was used to determine the composition of saccharides. Low concentration (from 50 to 1000 µg/mL) of decoction after 24 h incubation caused a significant increase in HGF cell viability. No cytotoxic effect was observed at any tested concentration (up to 2000 µg/mL). The lowest active concentration of decoction (50 µg/mL) was selected for further experiments. It significantly stimulated human gingival fibroblasts to proliferate, migrate, and increase the synthesis of collagen III. Phytochemical analysis showed significantly fewer polyphenols in the decoction than in the ethanol and acetone extracts tested earlier. In contrast, high levels of polysaccharides were observed. In our opinion, they may have a significant effect on the oral wound healing parameters analyzed in vitro. The results obtained encourage the use of this raw material in its traditional, safe form—decoction. [ABSTRACT FROM AUTHOR]

Background Scutellaria barbata D. Don (SB) is a widely used herbal medicine in China, with various pharmacological effects such as anti-oxidation, anti-inflammation, and anti-cancer. This work is aimed to investigate the tumor-suppressive effect of SB in cervical cancer (CC) and to identify its underlying mechanisms. Methods and materials CC cell lines (HeLa and HT-3) were treated with different concentrations of SB chloroform extract (ECSB) (0, 0.2, 0.5 mg/ml). MiR-195-5p and LOXL2 mRNA expression in CC cell lines and tissue samples was detected by quantitative real-time polymerase chain reaction. Cell counting kit-8 experiment was utilized to examine cell viability; TUNEL assay and Transwell experiment was executed to examine cell apoptosis, migration, and invasion. Western blotting experiments were implemented to detect LOXL2 protein expression. Bioinformatics and dual-luciferase reporter gene experiment were executed to examine the binding relationship between miR-195-5p and LOXL2. Results ECSB repressed the viability, migration, and invasion of HeLa and HT-3 cells, and promoted cell apoptosis in a dose-dependent manner. MiR-195-5p was remarkably under-expressed in CC tissues and cells, and ECSB up-regulated miR-195-5p expression. MiR-195-5p inhibitors partially counteracted the suppressive effects of ECSB on the malignant phenotypes of HeLa and HT-3 cells. LOXL2 was a downstream target of miR-195-5p, and ECSB up-modulated LOXL2 expression by specifically repressing miR-195-5p. Conclusion SB restrains CC cell proliferation and metastasis and promotes cell apoptosis via miR-195-5p/LOXL2, which may be a potential therapeutic agent for CC treatment. [ABSTRACT FROM AUTHOR]

Gallbladder cancer (GBC) is one of the lethal cancers with an extremely poor prognosis. In the recent 20 years, research on GBC has developed rapidly. Here we aim to perform a systematical bibliometric analysis on the current foci and status of GBC research. This study analyzes trends in GBC research and compares contributions from different countries and regions, institutions, and authors. All publications in GBC research from 2001 to 2021 in the Web of Science Core Collection (WoSCC) database were collected. Microsoft Excel 2010 and GraphPad Prism 9 were used to analyze publication data and publication trends. VOSviewer 1.6.17 was adapted to generate a visual network of keywords in surgical training research. A total of 3,323 publications were included. China was the most productive country, with the highest number of publications (n = 900, 27.08%). Shanghai Jiaotong University and Roa JC were the most productive institution and authors, contributing 215 and 89 publications, respectively. Keywords were classified into five clusters, each representing a key topic. The main clusters of GBC are related to surgery therapy, mechanism research-related study, and non-surgery therapy, while migration is the current hotspot of GBC research. The scientific progression of GBC research over the past two decades was comprehensively analyzed by this bibliometric study. Finding deeper mechanisms in the migration of GBC cells, new biomarkers, and highly effective nomograms will be the major problems and directions in the future. [ABSTRACT FROM AUTHOR]

Background. Esophageal cancer is one of the most lethal tumors worldwide. The most common histological type in China is esophageal squamous cell carcinoma (ESCC), accounting for 90% of cases. Esophageal cancer occurs at a high incidence in certain areas, among which China has the highest incidence. Although various therapeutic strategies have been used in clinical treatment, the 5-year survival rate is still not satisfactory, as it is only 15--20%. The reason for the poor prognosis of ESCC is that the distant metastasis easily occurs in these tumors. However, the mechanism of metastasis has not been studied clearly. Objectives. To investigate the function of hypoxia-inducible factor-2α (hif-2α) in ESCC. Materials and methods. Immunohistochemistry and immunofluorescence were used to detect the expression of hif-2α in tissues and cells. Clinicopathological data from 100 ESCC patients were used to investigate the relationship between hif-2α and prognosis. Cell experiments (Cell Counting Kit-8 (CCK-8) assay and transwell migration assays) were utilized to verify the roles of hif-2α on the ESCC cells. Western blotting was used to explore the mechanism of hif-2α in ESCC. Mouse model was used to clarify the effect of hif-2α on ESCC cells in vivo. Results. The hif-2α was overexpressed both in ESCC tissues and cells, and was related with poor prognosis in ESCC patients. The CCK-8 assay evidenced that silencing hif-2α suppressed the proliferation of ESCC cells, while transwell assay -- that overexpression of hif-2α promoted the migration of ESCC cells. Western blot assay indicated that hif-2α regulated epithelial--mesenchymal transition (EMT) through Notch pathway in ESCC cells. Mouse model showed that silencing hif-2α significantly suppressed the proliferation of ESCC cells in vivo. Conclusions. The hif-2α promotes EMT in ESCC through the Notch pathway. [ABSTRACT FROM AUTHOR]

Purpose. We previously reported that G protein-coupled receptor kinase (GRK) 4 halts cell cycle progression and induces cellular senescence in HEK293 cells. The present study was aimed at assessing the prognostic value of GRK4 in hepatocellular carcinoma (HCC). Methods. GRK4 expression was detected by immunohistochemistry in paired tumoral and peritumoral tissues of 325 HCC patients. One hundred and twenty-six patients from Western China were utilized as a training cohort to develop a nomogram, while 86 patients from Eastern China were used as a validation cohort. The proliferation and migration of lentiviral-GRK4 expressing HepG2 cells were determined by MTT and wound healing assays. Results. GRK4 was differentially expressed in HCC tissues. Tumoral GRK4 intensity, tumor type, and T stage were independent prognostic factors and used to form a nomogram for predicting overall survival (OS), which obtained a good concordance index of 0.82 and 0.77 in training and validation cohort, respectively. The positive and negative prediction values with nomogram were, respectively, 83% and 75% in training cohort and 100% and 52% in validation cohort. Patients with nomogram scores > 32 and 78 showed high risk for OS. Proliferation and motility capabilities were significantly restrained in GRK4-overexpressing HCC cells. Discussion. Low GRK4 expression in HCC tumor tissues indicates poor clinical outcomes. A prognostic nomogram including tumoral GRK4 expression would improve the predictive accuracy of OS in HCC patients. We also demonstrated that GRK4 overexpression inhibits proliferation and migration of HCC cells. The molecular mechanism underlying is worth further study. [ABSTRACT FROM AUTHOR]

Background. Small-molecule tyrosine inhibitor anlotinib which developed in China has been approved as a third-line treatment for patients with small-cell lung cancer (SCLC). Our previous clinical study found that anlotinib combined with S-1 has better short-term ORR than the single-agent anlotinib of SCLC and other small-molecule vascular targeted drug therapies in the treatment of SCLC. However, the molecular mechanism of those effect remains unclear. Methods. SCLC cell line H446 was treated with either anlotinib, 5-FU alone, or combination. The cellular effects including cell viability, cell apoptosis, cell cycle, cell migration, and invasion were explored to evaluate the cell proliferation level. Western blot was performed to determine the protein levels of the combined action of the two drugs. The xenograft mouse model was established by injection of H446 cells into mouse, and the animals were randomized and assigned for the drug treatments. Body weights and tumor sizes were recorded. WB was conducted using tumor tissues. All data were collected and statistically analyzed using t -test to reveal the underlying molecular mechanism. Results. When anlotinib was combined with 5-FU, the IC50 value of cells was significantly reduced. And apoptosis, cell cycle arrest, and cell motility rates were stronger when anlotinib combined with 5-FU than in the anlotinib or 5-FU alone. In H446 cell-derived xenograft mouse model, tumor volumes were significantly decreased in Anlo/5-FU combination group than anlotinib or 5-FU alone group. Western blot showed the decreasing expression of p-Src/p-AKT in the Anlo/5-FU group. Conclusion. Our data revealed that the treatment of combination of antitumor angiogenesis agent anlotinib with chemotherapy drug 5-FU may have synergistic cytotoxicity to SCLC in vitro and in vivo. This treatment modality reduced cell proliferation and migration via Src/AKT pathway. This new strategy may be a promising treatment for SCLC but needs to be confirmed in future clinical trials. [ABSTRACT FROM AUTHOR]

Background: Knee osteoarthritis (KOA) is one of the most common chronic musculoskeletal disorders worldwide, for which exosomes derived from stem cells may provide an effective treatment. Purpose: To assess the effect of exosomes derived from human urine–derived stem cells (hUSCs) overexpressing miR-140-5p (miR means microRNA) on KOA in an in vitro interleukin 1β (IL-1β)–induced osteoarthritis (OA) model and an in vivo rat KOA model. Study Design: Controlled laboratory study. Methods: Exosomes derived from hUSCs (hUSC-Exos) were isolated and validated. The hUSCs were transfected with miR-140s using lentivirus, and exosomes secreted from such cells (hUSC-140-Exos) were collected. The roles of hUSC-Exos and hUSC-140-Exos in protecting chondrocytes against IL-1β treatment were compared by analyzing the proliferation, migration, apoptosis, and secretion of extracellular matrix (ECM) in chondrocytes. After vascular endothelial growth factor A (VEGFA) was identified as a target of miR-140, the mechanism by which VEGFA can mediate the beneficial effect of miR-140 on OA was investigated using small interfering RNA transfection or chemical drugs. The expression of VEGFA in cartilage and synovial fluid from patients with KOA was measured and compared with that of healthy controls. Surgery for anterior cruciate ligament transection and destabilization of the medial meniscus were performed on the knee joints of Sprague-Dawley rats to establish an animal model of OA, and intra-articular (IA) injection of hUSC-Exos or hUSC-140-Exos was conducted at 4 to 8 weeks after the surgery. Cartilage regeneration and subchondral bone remodeling were evaluated through histological staining and micro–computed tomography analysis. Results: Proliferation and migration ability were enhanced and apoptosis was inhibited in chondrocytes treated with IL-1β via hUSC-Exos, with the side effect of decreased ECM secretion. hUSC-140-Exos not only retained the advantages of hUSC-Exos but also increased the secretion of ECM by targeting VEGFA, including collagen II and aggrecan. Increased expression of VEGFA during the progression of KOA was also confirmed in cartilage and synovial fluid samples obtained from patients with OA. In the rat OA model, IA injection of hUSC-140-Exos enhanced cartilage regeneration and subchondral bone remodeling. Conclusion: Our results demonstrated the superiority of hUSC-Exos overexpressing miR-140-5p for treating OA compared with the hUSC-Exos. The effect of hUSC-140-Exos for suppressing the progression of KOA is in part mediated by VEGFA. Clinical Relevance: Exosomes derived from stem cells may provide a promising treatment for KOA, and our study can advance the related basic research. [ABSTRACT FROM AUTHOR]

Background. Traditional Chinese medicine Smilax is the rhizome of liliaceous plant Smilax china L., which is used to treat pelvic inflammatory disease and anxieties. Purpose. To investigate the mechanism of anti-inflammatory activity of the extract from Smilax china L. (ES). Methods. The components of ES were identified by UPLC-QTOF-MS/MS. The anti-inflammatory activities were evaluated in xylene-induced ear oedema and egg white-induced plantar swelling test. Cell viability was examined by CCK-8 assay. The inflammatory mediators, proinflammatory cytokines, and MAPK and NF-κB signals in LPS-stimulated THP-1 cells were determined using ELISA, real-time PCR, and Western blot, respectively. Results. 20 compounds of ES were confirmed by comparing with the reference substance. ES displayed more prominent anti-inflammatory activity than the positive control "Jin Gang Teng" capsule in the in vivo acute inflammatory model. ES suppressed the expression of PGE2 and 6-Keot-PGF1α, and the ratio of IC50 (COX-1)/IC50 (COX-2) of ES was 3.15, which indicated that ES could selectively inhibit COX-2. ES dose-dependently (12.5, 25, and 50 mg/L) decreased the production and mRNA levels of proinflammatory cytokines IL-1β, IL-6, and TNF-α. Furthermore, ES significantly decreased LPS-induced phosphorylation of p38, JNK, ERK1/2, and p65, inhibiting the expression of IKKα and the degradation of IκBα. Conclusion. The results suggested that ES could selectively inhibit the activity of COX-2, and the anti-inflammatory effect of ES was associated with the inhibition of IL-1β, IL-6, and TNF-α via negative regulation of MAPK and NF-κB signaling pathways in LPS-induced THP-1 cells. [ABSTRACT FROM AUTHOR]

Copyright of Mycosystema is the property of Mycosystema Editorial Board 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.)

Background: Bladder cancer is having a gradually increasing incidence in China. Except for the traditional chemotherapy drugs, there are no emerging new drugs for almost 30 years in bladder cancer. New potential therapeutic targets and biomarkers are urgently needed. Methods: BORA is the activator of kinase Aurora A and plays an important role in cell cycle progression. To investigate the function of BORA in BCa, we established BORA knockdown and overexpression cell models for in vitro studies, xenograft and pulmonary metastasis mouse models for in vivo studies. Results: Our results indicated that BORA was upregulated in human bladder cancer (BCa) compared to the normal bladder and paracancerous tissues at transcriptional and translational levels. We found that BORA was positively related to BCa cell proliferation. Furthermore, BORA knockdown induced cell cycle arrest in G2/M phase while BORA overexpression decreased the proportion of cells in G2/M, associated with PLK1–CDC25C–CDK1 alteration. Interestingly, we observed that knockdown of BORA inhibited BCa cell migration and invasion, accompanied with alterations of epithelial–mesenchymal transition (EMT) pathway related proteins. In vivo studies confirmed the inhibition effect of BORA knockdown on BCa cell growth and migration. Conclusions: Our study indicates that BORA regulates BCa cell cycle and growth, meanwhile influences cell motility by EMT, and could be a novel biomarker and potential therapeutic target in BCa. [ABSTRACT FROM AUTHOR]

The Haplopelma hainanum is a species of theraphosid spider from China. Its large size and charming appearance make this species a popular pet. According to a previous study, theraphosid spider bites can induce pain, erythema, and edema in humans and can present more severely in domestic animals. The pathological consequences of envenomation by H. hainanum remain unclear. In this study, we investigated the effects and mechanisms of H. hainanum envenomation in mice. We showed that the venom induced slight swelling, intense inflammatory response, and increased the microvascular density in mice skin. Moreover, we found that 50 mg/ml of the spider's venom induced IL-1β expression in both HaCaT cells and fibroblast cells, but repressed CXCL10 expression in fibroblasts. The venom significantly induced cell senescence and repressed cell proliferation and migration in both HaCaT cells and fibroblast cells. Finally, we examined the expression of Nav channel in HaCaT and fibroblast cells and found that H. hainanum venom effectively inhibited NaC currents in HaCaT cells. Our study calls for further investigation of the pathological consequences and potential mechanisms of H. hainanum envenomation. This information might assist in the development of suitable therapy. [ABSTRACT FROM AUTHOR]

Aimin Zang,1 Zhiyu Wang,1 Guotao Fang,1 Dan Hong11Hebei Key Laboratory of Cancer Radiotherapy and Chemotherapy, Department of Medical Oncology, Affiliated Hospital of Hebei University, Baoding City, Hebei Province 071000, People's Republic of China; 2Department of Medical Pathology, Affiliated Hospital of Hebei University, Baoding City, Hebei Province 071000, People's Republic of China*These authors contributed equally to this workCorrespondence: Dan HongHebei Key Laboratory of Cancer Radiotherapy and Chemotherapy, Department of Medical Oncology, Affiliated Hospital of Hebei University, No. 648 Dongfeng East Road, Lianchi District, Baoding City, Hebei Province 071000, People's Republic of ChinaTel +86 31 2598 3042Email inaqhpnzgici45@163.com Purpose: It is widely known that some specific microRNAs can regulate the expressions of genes in gastric cancer cells at the post-transcriptional level. Previous studies have identified that miRNA-4766-5p was involved in tumor cell proliferation and can be an independent prognostic indicator for malignant pleural mesothelioma. However, the mechanism underlying gastric cancer via the miRNA-4766-5p pathway remains to be blank. Methods: We investigated the expression of miR-4766-5p in gastric cancer tissues and cells through qRT-PCR. We used RNAi to change the expressions of miR-4766-5p in gastric cancer cell lines, AGS and MKN45. Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to detect the mRNA expression of miR-4766-5p. We identified cell proliferation by CCK8 and clone formation assays. We analyzed the cell apoptosis and cycle through flow cytometry. At last, we used a dual-luciferase reporter assay to illustrate the interaction between miR-4766-5p and NKAP and used Western blot to determine the protein expression of signaling pathways. Results: We found that 1) miR-4766-5p was down-regulated in gastric cancer tissues and cells lines; 2) miR-4766-5p inhibited cell proliferation of gastric cancer cell lines significantly; 3) miR-4766-5p significantly inhibited cell migration and invasion of gastric cancer cells; 4) miR-4766-5p induced gastric cancer cell apoptosis. 5) NKAP was a direct target gene of miR-4766-5p; and 6) miR-4766-5p induced inactivation of AKT/mTOR pathway. Conclusion: The above results indicate that miR-4766-5p suppressed the proliferation and metastasis of gastric cancer cells through targeting NKAP. Our findings could probably contribute to the diagnostics and prognostics of gastric cancer through new methodologies. [ABSTRACT FROM AUTHOR]

AbstractAim:To explore a novel function of a mutant of the hepatitis B virus X protein (HBxΔ127) in the promotion of hepatoma cell migration.Methods:The effect of HBxΔ127 and wild type HBx on the migration ability of hepatoblastoma HepG2 cells were examined using wound healing assays in stable transfection systems. The full-length osteopontin(OPN) promoter sequence was cloned into the pGL3-Basic plasmid. The promoter activities of OPN in stably HBxΔ127-transfected hepatoblastoma HepG2 (HepG2-XΔ127) and hepatocellular carcinoma H7402 (H7402-XΔ127) cells were determined using luciferase reporter gene assays. The mRNA expression levels of OPN were detected by RT-PCR. And the effect of MK886, a specific inhibitor of 5-lipoxygenase (5-LOX), on OPN promoter activity and mRNA expression in HepG2-XΔ127 and H7402-XΔ127 cells were examined using luciferase reporter gene assays and RT-PCR, respectively. Finally, the migration ability of HepG2-XΔ127 was observed after treatment with siRNA targeting OPN mRNA and HBx mRNA using wound healing assays.Results:HepG2-XΔ127 cells exhibited a greater capacity for wound repair compared to HepG2-X cells. The promoter activity and mRNA expression levels of OPN were also increased in HepG2-XΔ127 and H7402-XΔ127 cells. Moreover, MK886 abolished the HBxΔ127-mediated upregulation of OPN. Wound healing assays demonstrated that the migration ability of HepG2-XΔ127 cells can be suppressed by treatment with siRNA targeting OPN mRNA and siRNA targeting HBx mRNA.Conclusion:HBxΔ127 strongly promotes hepatoma cell migration via activation of OPN involving 5-LOX. [ABSTRACT FROM AUTHOR]

Background: Monoamine oxidase (MAO) A catalyzes oxidative deamination of monoamine neurotransmitters and dietary amines and regulates brain development and functions. Recently, we showed that MAO A mediates the progression and migration of glioma and MAO A inhibitors reduce glioma cell growth. Glioblastoma (GBM) is a common and most malignant brain tumor which is difficult to treat. Temozolomide (TMZ) is the current standard chemotherapy for glioma, but tumors usually become resistant and recur. So far, no effective therapy for TMZ-resistant glioma is available. Natural plant antimicrobial solution (PAMs) is a Chinese herbal medicine which has been used for decades without toxicity and has multiple medical functions including anti- inflammatory effects. Here, we report the effects of PAMs on glioblastoma growth. Methods: The growth of TMZ -sensitive (U251S),-resistant (U251R) human glioma cells, and mouse glioma cell line GL-26 were assessed by MTS colorimetric assay, colony formation, and cell migration assays. Male C57BL/6 mice were implanted subcutaneously or intracranial with luciferase-positive mouse glioma GL-26 cells and treated with vehicle; MAO A inhibitor clorgyline (10 mg/kg); TMZ (1 mg/kg); PAMs (48 mg/kg) alone or in combination with TMZ (1 mg/kg) for 14 days. At the end of the treatment, mice were sacrificed, MAO A catalytic activity in tumors was measured, and tumor sizes were determined by imaging and weight. Results: These results show that PAMs inhibits MAO A catalytic activity in all three glioma cell lines studied U251S, U251R, and GL-26. PAMs reduced glioma growth and has greater effects in combination with low dose of TMZ than PAMS or TMZ alone in all three cell lines as shown by MTS, colony formation, and cell migration assays. Using the subcutaneous or intracranial GL-26 glioma mouse model, PAMs reduced the tumor growth and MAO A activity, similar to the MAO A inhibitor clorgyline. Combining PAMs with non-toxic dose TMZ increased survival to a greater extent than those of PAMs or TMZ alone. Conclusions: This is the first study which suggests that PAMs alone or co-administration with low doses of TMZ may be a potential adjuvant to reduce the toxicity of TMZ and to abrogate drug resistance for the effective treatment of glioma. [ABSTRACT FROM AUTHOR]

Background: Breast cancer is the leading cause of cancer-related death in women worldwide. Although traditional Chinese medicine (TCM) is commonly used by patients with breast cancer, little is known about TCM prescriptions for breast cancer. This study investigated the effects of a new TCM formula, T33, comprising Radix Kansui, Rheum rhabarbarum, Paeonia lactiflora, Jiangbanxia, and Zhigancao on breast cancer cells in vitro and in vivo. Methods: To evaluate the effects of T33 on human breast cancer, HMEpiC, MDA-MB231 and MCF-7 cells were treated with different concentrations of T33 and then analyzed using MTT and Transwell migration assays. To elucidate the involvement of autophagy in the T33-induced death of MDA-MB231 and MCF-7 cells, immunofluorescence staining with LC3-II-specific antibodies was performed. Tumor xenografts were generated by subcutaneously injecting either MDA-MB231 or MCF-7 cells into BALB/c nude mice to determine the effects of T33 on these cell lines in vivo. Results: The experimental results revealed that 0.1 mg/mL, 0.5 mg/mL, 2.5 mg/mL, 5 mg/mL and 10 mg/mL T33 significantly inhibited the proliferation and invasion of MDA-MB231 and MCF-7 cells. Moreover, significant autophagy was observed in MDA-MB231 and MCF-7 cells in the presence of 2.5 mg/mL, 5 mg/mL and 10 mg/mL T33. An animal study further revealed that both low (200 mg/kg) and high (600 mg/kg) doses of T33 inhibited the proliferation of xenografted breast cancer cells in BALB/c nude mice. Conclusion: These findings demonstrate for the first time that T33 has potential in the treatment of breast cancer owing to its antiproliferative effects and induction of autophagy. [ABSTRACT FROM AUTHOR]