Abstract
Background miR-206 was reported to be a tumor suppressor in bladder cancer. In this study, we explore the expression and function of miR-206 in endometriosis (EM). Methods 40 EM patients undergoing total hysterectomy were selected as the experimental group. RT-qPCR assay was adopted to detect the expression of MALAT1 and miR-206 in EM. Cell proliferation was detected by EdU incorporation and colony formation assay. Cell migration and invasion viability of ESCs were examined by transwell assay and wound healing assay. Flow cytometry was carried out to assess cell apoptosis of ESCs. The protein expressions of Bcl-2 and Bax were examined by western blot assay. The relationship between miR-206 and MALAT1 was verified by the dual-luciferase reporter assay and RNA pull-down assay. Results In this work, miR-206 was found to be downregulated in EM. Functional experiments displayed that miR-206 mimic repressed cell proliferation, migration, and invasion of ESCs and promoted cell apoptosis of ESCs. Furthermore, miR-206 mimic reduced the expression of Bcl-2 but enhanced the expression of Bax. MALAT1 was found to be upregulated in EM. Furthermore, MALAT1 was indicated to be a target of miR-206. Additionally, MALAT1 was found to alleviate the influence of miR-206 on cell progression of ESCs. Furthermore, miR-206 inhibited tumor growth in vivo. Conclusion This study indicated that miR-206 inhibited cell progression by regulating MALAT1 in EM. Hence, miR-206 was suggested to be a possible target for EM treatment.
Highlights
Endometriosis (EM) refers to the infiltration and growth of endometrial tissue outside the uterus [1]
Clinical Samples. e ectopic endometrial tissues of 40 EM patients undergoing total hysterectomy were selected as the experimental group
After transfection for 48 h, cells were added with lysate and centrifuged at 10000 r/min for 10 min to obtain total protein. e protein was wettransferred to PVDF membrane after SDS-PAGE electrophoresis. e membrane was immersed in the primary antibodies at 4°C overnight. en, the secondary antibodies were incubated for 1 h at room temperature. e primary antibodies were anti-β-actin (1 : 1000, #12620, Cell Signaling Technology, MA, USA), anti-Bcl-2 (1 : 1000, #3498, Cell Signaling Technology, MA, USA), anti-Bax (1 : 1000, 14796S, Cell Signaling Technology, MA, USA). e secondary antibodies were anti-rabbit IgG (1 : 2000, #14708, Cell Signaling Technology, MA, USA)
Summary
Endometriosis (EM) refers to the infiltration and growth of endometrial tissue outside the uterus [1]. MiR-206 was reported to suppress cell migration by downregulating EGFR expression in liver cancer [6]. MiR-206 promoted mammary differentiation and accumulation of related lipids in breast cancer [7]. MiR-206 was at a low level in cervical cancer (CC) and suppressed CC cell invasion, migration, and growth by modulating BAG3 [8]. Journal of Healthcare Engineering lncRNAs are functional RNA molecules over 200 nt in length, lacking the ability to encode proteins and regulating gene expression at various levels [9]. Bai et al found 1474 differentially expressed lncRNAs in EM by bioinformation technology, and the expressions of RP1196D and GS1-358P8.4 were closely related to EM cell progression [10]. LncRNA MALAT1 is involved in regulation of gene expression before and after transcription. The effect of miR-206/MALAT1 on EM progression was investigated. MiR-206 was suggested to be an effective target for EM treatment
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