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 wa...

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Main Authors: Yan Li, Jinhua Zhou, Juan Wang, Xiaoping Chen, Yan Zhu, Youguo Chen
Format: Article
Language:English
Published: BMC 2020-03-01
Series:Biological Research
Subjects:
Online Access:http://link.springer.com/article/10.1186/s40659-020-00277-4
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author Yan Li
Jinhua Zhou
Juan Wang
Xiaoping Chen
Yan Zhu
Youguo Chen
author_facet Yan Li
Jinhua Zhou
Juan Wang
Xiaoping Chen
Yan Zhu
Youguo Chen
author_sort Yan Li
collection DOAJ
description 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.
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spelling doaj.art-852f44d5a9704bb7a0e8332cfc8f77e92022-12-22T00:05:18ZengBMCBiological Research0717-62872020-03-015311810.1186/s40659-020-00277-4Mir-30b-3p affects the migration and invasion function of ovarian cancer cells by targeting the CTHRC1 geneYan Li0Jinhua Zhou1Juan Wang2Xiaoping Chen3Yan Zhu4Youguo Chen5Department of Obstetrics and Gynecology, The First Affiliated Hospital of Soochow UniversityDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Soochow UniversityDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Soochow UniversityDepartment of Obstetrics and Gynecology, The First People’s Hospital of YanchengDepartment of Obstetrics and Gynecology, The First People’s Hospital of YanchengDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Soochow UniversityAbstract 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.http://link.springer.com/article/10.1186/s40659-020-00277-4miR-30b-3pOvarian cancerOVCAR3CTHRC1EMT
spellingShingle Yan Li
Jinhua Zhou
Juan Wang
Xiaoping Chen
Yan Zhu
Youguo Chen
Mir-30b-3p affects the migration and invasion function of ovarian cancer cells by targeting the CTHRC1 gene
Biological Research
miR-30b-3p
Ovarian cancer
OVCAR3
CTHRC1
EMT
title Mir-30b-3p affects the migration and invasion function of ovarian cancer cells by targeting the CTHRC1 gene
title_full Mir-30b-3p affects the migration and invasion function of ovarian cancer cells by targeting the CTHRC1 gene
title_fullStr Mir-30b-3p affects the migration and invasion function of ovarian cancer cells by targeting the CTHRC1 gene
title_full_unstemmed Mir-30b-3p affects the migration and invasion function of ovarian cancer cells by targeting the CTHRC1 gene
title_short Mir-30b-3p affects the migration and invasion function of ovarian cancer cells by targeting the CTHRC1 gene
title_sort mir 30b 3p affects the migration and invasion function of ovarian cancer cells by targeting the cthrc1 gene
topic miR-30b-3p
Ovarian cancer
OVCAR3
CTHRC1
EMT
url http://link.springer.com/article/10.1186/s40659-020-00277-4
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