Effects of miR-211-3p/RHBDD1 axis on cell proliferation, cell cycle progression, and epithelial-mesenchymal transition in glioma
This study was designed to elucidate the relationship of miR-211-3p and rhomboid domain containing 1 (RHBDD1) in glioma. Here, we first observed that miR-211-3p directly targets the 3˘-UTR of RHBDD1 in glioma cells using dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay, reverse tr...
Main Authors: | , , , , , |
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Format: | Article |
Language: | English |
Published: |
Termedia Publishing House
2022-06-01
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Series: | Folia Neuropathologica |
Subjects: | |
Online Access: | https://www.termedia.pl/Effects-of-miR-211-3p-RHBDD1-axis-on-cell-proliferation-r-ncell-cycle-progression-and-epithelial-mesenchymal-transition-r-nin-glioma,20,47508,1,1.html |
Summary: | This study was designed to elucidate the relationship of miR-211-3p and rhomboid domain containing 1 (RHBDD1) in glioma. Here, we first observed that miR-211-3p directly targets the 3˘-UTR of RHBDD1 in glioma cells using dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay, reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and Western blot analysis. Pearson’s correlation analysis showed that miR-211-3p expression was negatively correlated with RHBDD1 expression in glioma tissues. CCK-8 assay, flow cytometry, and transwell assay were applied to assess cell proliferation, cell cycle distribution, migration, and invasion. The results showed that RHBDD1 knockdown inhibited cell proliferation, cell cycle G1/S transition, migration, and invasion in two glioma cell lines (U87 and LN-229). Knockdown of miR-211-3p obtained opposite results. Moreover, overexpression of RHBDD1 counteracted suppressive effects of miR-211-3p on glioma cells. Furthermore, decreased expression of CDK4, cyclin D1, N-cadherin, and vimentin as well as increased E-cadherin expression induced by miR-211-3p was reversed by RHBDD1 overexpression. Our results suggested that targeting miR-211-3p/RHBDD1 axis might be a novel effective therapeutic target for glioma treatment. |
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ISSN: | 1641-4640 1509-572X |