Search

Non‐small cell lung cancer (NSCLC) is one of the most common malignant tumors worldwide. Circular RNAs (circRNAs) have been widely reported to play a role in the pathogenesis of various tumors. Nevertheless, the function of circ_0001955 in NSCLC progression has not been explored yet. This study aims to explore the functions of circ_0001955 in NSCLC and investigate its regulatory molecular mechanism. First, we determined that circ_0001955 was upregulated in NSCLC cells. Subsequently, we demonstrated that knockdown of circ_0001955 restrained cell proliferation and invasion. In vivo experiments further proved the suppressive effect of circ_0001955 silence on tumor growth. Mechanism assays revealed that circ_0001955 enhanced nuclear factor‐κB (NF‐κB) inhibitor interacting Ras‐like protein 2 (NKIRAS2) expression by sponging microRNA‐29a‐3p (miR‐29a‐3p). Upregulation of NKIRAS2 led to the deceased level of IκBβ but increased levels of nuclear p65, thus activating the NF‐κB signaling pathway. In conclusion, Circ_0001955 activates the NF‐κB pathway to promote NSCLC cell proliferation and invasion by regulating miR‐29a‐3p/NKIRAS2 axis. [ABSTRACT FROM AUTHOR]

Eicosapentaenoic acid (EPA) has been reported to play an anti‐inflammatory and antioxidative stress role in a series of human diseases, including major depressive disorder. However, its exact mechanism is still largely unknown. Mouse BV‐2 cells were treated with lipopolysaccharide (LPS) to induce an in vitro inflammatory cell model of depression. Cytotoxic effects were assessed with MTT and lactate dehydrigebase release assays. Cytokine mediators were elevated by western blot and enzyme‐linked immunosorbent assays. Autophagy‐relators were determined by immunofluorescence and western blot analyses. Interaction relationships among molecules were evaluated utilizing chromatin immunoprecipitation and dual luciferase assays. Methylated miR‐29a‐3p was detected via methylation‐specific polymerase chain reaction. EPA treatment at 60 μM had no cytotoxic effects on BV2 cells and significantly inhibited the LPS‐induced inflammatory response and NLRP3 inflammasome but activated autophagy, while all these effects were reversed by the autophagy inhibitor 3‐MA. Importantly, miR‐29a‐3p exhibited a role similar to that of EPA in LPS‐treated BV2 cells. Mechanistically, EPA treatment elevated miR‐29a‐3p by repressing its promoter methylation. MAPK8 was a direct target of miR‐29a‐3p. Inhibition of miR‐29a‐3p greatly diminished the regulatory roles mediated by EPA in LPS‐treated BV2 cells, while these roles were further impeded after MAPK8 silencing. To conclude, our data demonstrated that EPA treatment alleviated LPS‐induced NLRP3 inflammasomes by activating autophagy via regulation of miR‐29a‐3p/MAPK8 signaling, which further elucidates the potential antidepressant mechanism of EPA. [ABSTRACT FROM AUTHOR]

Background: With the promotion of human papillomavirus (HPV) vaccine, cervical cancer has become a current research hotspot, and lncRNA has been confirmed to be used in the research of different diseases. This article systematically expounds the regulation and potential mechanisms of HOXA cluster antisense RNA 3 (HOXA‐AS3) in cervical cancer, and discusses its possibility as a prognostic biomarker for cervical cancer. Methods: Relative expression levels of HOXA‐AS3 and miR‐29a‐3p in tissues and cells were determined by real‐time quantitative polymerase chain reaction (RT‐qPCR). The survival of cervical cancer patients was analyzed by Kaplan–Meier method and the cumulative survival function table was drawn. The proliferation, migration, and invasion levels of HOXA‐AS3 in cells were detected according to cell counting kit‐8 (CCK‐8) and transwell method. The dual‐luciferase reporter gene assay confirmed the mechanism of action between HOXA‐AS3 and miR‐29a‐3p. Results: HOXA‐AS3 was elevated and miR‐29a‐3p was decreased in tissues and cells of cervical cancer patients. Knockdown of HOXA‐AS3 could inhibit the progression of cervical cancer and was more conducive to patient survival. Bioinformatics analysis confirmed that HOXA‐AS3 negatively regulates cervical cancer development by sponging miR‐29a‐3p. Conclusion: In this research, knockdown of HOXA‐AS3 could alleviate the process of cervical cancer by sponging miR‐29a‐3p, suggesting that HOXA‐AS3 may be a potential prognostic target of cervical cancer, which could provide a theoretical basis for future clinical research of cervical cancer. [ABSTRACT FROM AUTHOR]

Background: Ameloblastoma (AB) is a common epithelial odontogenic tumor. The Wnt/β‐catenin pathway has been found to be related to AB invasion. Methods: The alteration expression of microRNAs (miRNAs) and messenger RNAs (mRNAs) was performed by miRNA and mRNA microarray analysis and validated by quantitative real‐time polymerase chain reaction (RT‐PCR). The effects of miR‐29a‐3p on migration and invasion in AB cells were evaluated by a transwell assay. Bioinformatic prediction was conducted using the miRSystem and validated by quantitative RT‐PCR, western blot, and a luciferase reporter assay. Results: miR‐29a‐3p was overexpressed in AB tissues, which promoted the migration and invasion of AB cells in vitro. Catenin beta interacting protein 1 (CTNNBIP1), a negative regulator of the Wnt/β‐catenin pathway, was predicted to be a target of miR‐29a‐3p. miR‐29a‐3p inhibited the expression of CTNNBIP1 and promoted the expression of the downstream molecules of the Wnt/β‐catenin pathway. Conclusions: miR‐29a‐3p promoted migration and invasion in AB via Wnt/β‐catenin signaling by targeting CTNNBIP1. [ABSTRACT FROM AUTHOR]

Circular RNA FOXO3 (CircFOXO3, also termed as Hsa_circ_0006404) is derived from exon 2 of forkhead box O3 (FOXO3) gene, and abnormal expression is shown in different diseases. However, whether circFOXO3 plays important roles in tumorigenesis and progression of prostate cancer (PCa) remains unclear. In this study, we found that circFOXO3 was up‐regulated in both PCa tissues and serum samples. Moreover, circFOXO3 was positively correlated with the Gleason score in PCa samples. CircFOXO3 was observed to be up‐regulated in Gleason score > 6 PCa samples compared with Gleason score = 6 PCa samples. Knock‐down circFOXO3 could remarkably inhibit PCa cell cycle, proliferation and promote cell apoptosis in vitro. Furthermore, we demonstrated circFOXO3 could act as miR‐29a‐3p sponge to up‐regulate SLC25A15 expression by bioinformatics analysis, dual‐luciferase reporter assays and biotinylated RNA pull‐down assays. SLC25A15 could reverse the tumour suppressing roles of knock‐down circFOXO3 in PCa. Of note, we found that miR‐29a‐3p was down‐regulated; however, SLC25A15 was overexpressed in PCa samples compared with normal tissues. In conclusion, circFOXO3 acts as a miR‐29a‐3p sponge to exhibit oncogenic activity that affects the cell cycle and cell apoptosis in PCa through transcriptional up‐regulation of SLC25A15. Our analysis suggests circFOXO3 could act as promising prostate cancer biomarkers. [ABSTRACT FROM AUTHOR]

MicroRNAs (miRNAs) are known to play a regulatory role in various cancers including laryngocarcinoma. MiR-29a-3p is a potential tumor-suppressive miRNA, but its function in laryngocarcinoma is unknown. The purpose of this study was to investigate the roles of miR-29a-3p in laryngocarcinoma. Prominin1 (PROM1) was predicted as a target gene of miR- 29a-3p and this was verified using a luciferase reporter assay. Transfection of miR-29a-3p into two laryngocarcinoma cell lines indicated that miR- 29a-3p could decrease cell proliferation and enhance the chemotherapy response by targeting PROM1. PROM1 expression was up-regulated in the laryngocarcinoma cells when miR-29a-3p was down-regulated. We found miR-29a-3p expression levels were lower in laryngocarcinoma tissues than in control tissues. We also found that miR-29a-3p expression was negatively correlated with PROM1 expression in laryngocarcinoma tissues. The study demonstrates that miR-29a-3p suppresses cell proliferation in laryngocarcinoma by targeting PROM1. [ABSTRACT FROM AUTHOR]

The aim of this study was to evaluate the role of the angiotensin II (Ang II) induced-differential mi RNA expression in renal glomerular and tubulo-interstitial fibrosis in an experimental model of Ang II-dependent hypertension. To clarify this issue, Sprague Dawley rats were treated with Ang II (200 ng/kg per minute, n = 15) or physiological saline ( n = 14) for 4 weeks. Systolic blood pressure and albuminuria were measured every 2 weeks. At the end of the experimental period, renal glomerular and tubulo-interstitial fibrosis was evaluated by histomorphometric analysis, after Sirius-Red and Masson's trichrome staining. Ang II increased systolic blood pressure ( P < 0.0001), albuminuria ( P < 0.01) and both glomerular and tubulo-interstitial fibrosis ( P < 0.01). Using laser capture microdissection and mi RNA microarray analysis this study showed that miR-29a-3p was down-regulated in renal tubules and up-regulated in glomeruli. Real-time polymerase chain reaction ( PCR) experiments confirmed in Ang II-treated rats a down-regulation of miR-29a-3p in tubules ( P < 0.01), while no significant changes were observed in glomeruli. Matrix metalloproteinase-2 ( MMP-2) was identified as putative miR-29a-3p target (by TargetScan, miRanda, Tarbase software) and functionally confirmed by luciferase activity assay. These data demonstrate that the effects of Ang II on miR-29a-3p expression in renal tubules is different from the one exerted in the glomeruli and that miR-29a-3p targets MMP-2. These results suggest that the development of renal fibrosis at glomerular and tubulo-interstitial level depends on different molecular mechanisms. [ABSTRACT FROM AUTHOR]