Mir-30b-3p affects the migration and invasion function of ovarian cancer cells by targeting the CTHRC1 gene

Abstract

Background: The aim of this study was to investigate the effect role and mechanism of miR-30b-3p on ovarian cancer cells biological function. Methods: The expression of miR-30b-3p was detected in ovarian cancer cell lines and normal ovarian epithelial cell line by qRT-PCR. Mir-30b-3p mimic was transfected into OVCAR3 cells. Cell-counting kit-8 (CCK-8) assay was conducted to explore the effect of mir-30b-3p on the OVCAR3 cells' proliferation. Cell cycle and apoptosis were detected by Flow cytometry. Cell invasion ability was detected by Transwell test. The regulation of putative target of miR-30b-3p was verified by double luciferase reporter assays and Western blot. Result: We found that miR-30b-3p was downregulated in OVCAR3 cells. Overexpression of miR-30b-3p suppressed proliferation, promoted apoptosis, slowed cell cycle and inhibited migration and invasion of OVCAR3 cells. Bioinformatics analysis identified 3′-untranslated region (3′UTR) of Collagen triple helix repeat-containing 1 (CTHRC1) as the presumed binding site for miR-30b-3p. Detection of double luciferase reporter and Western-Blot result confirmed that CTHRC1 was the target gene of miR-30b-3p. Furthermore, E-cadherin, β-cadherin and Vimentin protein expression level were changed after transfection of miR-30b-3p. Conclusion: miR-30b-3p function as an anti-cancer gene. Overexpression of miR-30b-3p can inhibit the biological function of ovarian cancer cells. MiR-30b-3p targets CTHRC1 gene plays an important role in epithelial-mesenchymal transformation (EMT), and supports miR-30b-3p as a potential biological indicator for ovarian cancer in the future.

Arbutin suppresses osteosarcoma progression via miR‐338‐3p/MTHFD1L and inactivation of the AKT/mTOR pathway

“…2). In addition, as we previously described [12], silencing MTHFD1L can suppress the activity of the AKT/mTOR pathway in OS cells. Thereby, we evaluated the AKT/mTOR pathway‐related protein levels to validate whether Arbutin treatment affects the activation of AKT/mTOR signaling.…”

“…[11] have confirmed that the repression of Arbutin to aggressive melanoma development is associated with the dysregulation of p53, ENOA and VIME. Based on our prior study, MTHFD1L has been concluded as a prospective therapeutic target for OS [12]. The Comparative Toxicogenomics Database (CTDbase) website analysis revealed that Arbutin treatment can decrease the expression of MTHFD1L.…”

WITHDRAWN: microRNA-4488 in extracellular vesicles derived from marrow mesenchymal stem cells suppresses ABHD8 to inhibit ovarian cancer progression

“…miR-644-5p over-expressed in BMSC-EVs protects the ovarian granulosa cells by targeting p53, contributing to recover the function of ovarian (24). Upregulated miR-30b-3p inhibits the OVCAR3 cell proliferation, migration, and invasion while enhancing the apoptosis in ovarian cancer (25).…”

microRNA-1271-5p/TIAM1 suppresses the progression of ovarian cancer through inactivating Notch signaling pathway

“…Paliwal et al illustrated that miR-22 and miR-21 are wonderful diagnostic indicators for OC early diagnosis [ 9 ]. miR-30b-3p as an anti-tumor gene in OC represses the migration and invasion of cells via down-regulating the CTHRC1 gene [ 10 ]. Among the massed miRNAs, miR-1271-5p is expressed at abnormal levels in many human cancers and participates in the tumorigenesis [ 11 , 12 ].…”