miR-182 inhibits proliferation, invasion of endometrial glandular epithelial cells in endometriosis micevia Wnt signaling pathway by targeting AQP5 / 中华内分泌外科杂志

Objective:To elucidate the effect of miR-182 on proliferation, invasionof endometrial glandular epithelial cells in endometrrosis (EMs) mice via Wnt signaling pathway through targeting Aquaporin5 (AQP5) .Methods:The mice model of EMs were established. Subsequently the adenoepithelial tissue of endometrium were collected and the expression of miR-182 and AQP5 in tissue was detected. Enzyme-linked immunosorbent assay (ELISA) was performed to test the expression of inflammatory factors in normal and EMs mice. Then endometrial glandular epithelial cells in mice were isolated and divided into different groups. qRT-PCR and Western blot was performed to detect the expression of miR-182, AQP5,and Wnt pathway related factors (Wnt-1, β-catenin) in cells. The proliferation activity and invasion ability in each group of cells were examined by MTT and Transwell.Results:Compared with Normal mice, the expression of miR-182 was decreased while AQP5 and Wnt pathway related factors (Wnt-1, β-catenin) expression were increased in endometrial glandular epithelial tissues of EMs mice (all P<0.05) . In cell experiments, miR-182 overexpression or AQP5 silencing could inhibit the expression of Wnt pathway related factors (Wnt-1, β-catenin) . At the same time, cell viability as well as invasion ability were decreased (all P<0.05) . Indexes in miR-182 inhibitor group exhibited an opposite trend compared with that in miR-182 mimic group. The effects of sh-AQP5 on EMs cells could be offset by miR-182 inhibitor. Conclusion:Up-regulated expression of miR-182 can reduce the proliferation and invasion of endometrial glandular epithelial cells of EMs mice through inhibiting the activation of Wnt signaling pathway by down-regulating AQP5.

miR-182 modulates cell proliferation and invasion in prostate cancer via targeting ST6GALNAC5

Altered expression of miR-182 has been observed in various types of human cancer. The purpose of this study was to investigate the expression of miR-182 and its role in prostate cancer (PCa). Expression of miR-182 and ST6GALNAC5 in tumor tissues and the Du145 PCa cell line was analyzed. Cell proliferation assay, colony formation assay, transwell assay, and wound healing assay were performed. The impact of miR-182 on tumor growth was investigated using a xenograft model. The results indicated that expression of miR-182 was higher in PCa tissues and cell lines, while ST6GALNAC5 was decreased. Downregulating miR-182 significantly inhibited the capacities of proliferation and invasion of PC3 and Du145 cells. ST6GALNAC5 was demonstrated to be a target of miR-182 by luciferase assay, and western blot results indicated PI3K/Akt pathway was involved in miR-182 associated effects on PC3 and Du145 cells. The animal experiment suggested that knockdown of miR-182 inhibited tumor growth. Our study proved that miR-182 participated in the proliferation and invasion of PCa cells via mediating expression of ST6GALNAC5 and established a miR-182/ST6GALNAC5/PI3K/AKT axis in regulation of tumor progression. Our investigation provided a basis for further exploration of the application of miR-182 or ST6GALNAC5-associated therapies for PCa patients.

Potential biomarkers in NASH-induced liver cirrhosis with hepatocellular carcinoma: A preliminary work on roles of exosomal miR-182, miR-301a, and miR-373

@#Introduction: Recent studies have published the roles of exosomal miRNAs in the pathogenesis of various type of malignancies and can be developed as potential biomarkers for diagnostic, prognostic and therapeutic purposes. The aim of this study was to identify the expression level of selected miRNAs (miR-182, miR-301a, and miR-373) in exosomes of the serum and ascitic fluid in patients with non-alcoholic steatohepatitis (NASH)-related liver cirrhosis with or without hepatocellular carcinoma (HCC). Materials and Methods: A literature search was performed to identify potential miRNAs involved in the pathogenesis of HCC. Unpaired serum and ascitic fluid were obtained from 52 patients with NASH related liver cirrhosis (n=26 for each group of with and without HCC). Exosomal miRNA was isolated from all samples. Expression levels of miR-182, miR-301a and miR373 were determined using quantitative real-time PCR. Results: Serum-derived exosomal mir-182, miR-301a and miR-373 were significantly up-regulated with fold change of 1.77, 2.52, and 1.67 (p< 0.05) respectively in NASH-induced liver cirrhosis with HCC as compared to NASH-induced liver cirrhosis without HCC. We identified the expression levels of ascitic fluid-derived exosomal mir-182, miR-301a, and miR-373 were significantly up-regulated with fold change of 1.6, 1.94 and 2.13 respectively in NASH-induced liver cirrhosis with HCC as compared to NASH-induced liver cirrhosis without HCC (p <0.05). There was poor correlation expression of all the selected exosomal miRNA between serum- and ascitic fluid-derived in HCC group. Conclusions: This preliminary data showed significant increase in the expression levels of exosomal miR-182, miR-301a and miR373 in both serum and ascetic fluid suggesting the possible roles of these miRNAs as circulating biomarkers for NASH-induced liver cirrhosis with hepatocellular carcinoma

MiR-182-5p Knockdown Targeting PTEN Inhibits Cell Proliferation and Invasion of Breast Cancer Cells

PURPOSE: Breast cancer (BC) is one of the most common malignant tumors, affecting a significant number of women worldwide. MicroRNAs (miRNAs) have been reported to play important roles in tumorigenesis. The aim of this study was to determine the roles of miR-182-5p in BC progression. MATERIALS AND METHODS: The expressions of miR-182-5p and phosphatase and tensin homolog deleted on chromosome 10 (PTEN) were measured in BC tissues and cells by quantitative real-time polymerase chain reaction or Western blot. Cell proliferation and invasion were detected by cell counting kit-8 assay and trans-well assay, respectively. The interaction between miR-182-5p and PTEN was probed by bioinformatics analysis, luciferase activity, and RNA immunoprecipitation. A murine xenograft model was established to investigate the role of miR-182-5p in BC progression in vivo. RESULTS: An abundance of miR-182-5p was noted in BC tissues and cells. High expression of miR-182-5p was associated with poor survival. Abrogation of miR-182-5p inhibited cell proliferation and invasion in BC cells. Interestingly, PTEN was indicated as a target of miR-182-5p, and its restoration reversed miR-182-5p-mediated promotion of proliferation and invasion of BC cells. Moreover, depletion of miR-182-5p suppressed tumor growth via up-regulating PTEN expression in the murine xenograft model. CONCLUSION: MiR-182-5p exhaustion blocked cell proliferation and invasion by regulating PTEN expression, providing a novel therapeutic avenue for treatment of BC.