CircWDR26 regulates endometrial carcinoma progression via miR-212-3p-mediated typing genes MSH2

Abstract Background Circular RNAs (circRNA) are important in mediating tumor progression, but their roles in endometrial carcinoma (EC) are not fully understood yet. Many circRNAs are dysregulated and may contribute to EC progression. The functions of circWDR26 in EC remain unknown. Methods The expr...

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Main Authors: Tao-Xiang Lei, De-Jian He, Jian Cao, Wang-Gui Lv
Format: Article
Language:English
Published: BMC 2022-07-01
Series:European Journal of Medical Research
Subjects:
Online Access:https://doi.org/10.1186/s40001-022-00755-3
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author Tao-Xiang Lei
De-Jian He
Jian Cao
Wang-Gui Lv
author_facet Tao-Xiang Lei
De-Jian He
Jian Cao
Wang-Gui Lv
author_sort Tao-Xiang Lei
collection DOAJ
description Abstract Background Circular RNAs (circRNA) are important in mediating tumor progression, but their roles in endometrial carcinoma (EC) are not fully understood yet. Many circRNAs are dysregulated and may contribute to EC progression. The functions of circWDR26 in EC remain unknown. Methods The expression of circWDR26 in EC and adjacent normal tissues, and cell lines was determined by qPCR. The proliferation, apoptosis, migration, and invasion of EC cells was examined by CCK-8 assay, flow cytometry, wound healing assay and Transwell assay. The interaction between circWDR26, MSH2 and miR-212-3p was determined by luciferase assay. EC cells were inoculated into nude mice and tumor burden was determined by measuring tumor dimensions, size, and weight. The proliferative marker Ki67 in EC tissue was determined by immunohistochemistry. Results The expression of circWDR26 in EC tissues or cell lines was higher than in the normal tissue or endometrial epithelial cells. Downregulation of circWDR26 resulted in attenuated proliferation, increased apoptosis, reduced migration and invasion of EC cells. Mechanistically, circWDR26 targeted and suppressed the expression of miR-212-3p. We further found that MSH2 was the novel target of miR-212-3p and was upregulated by circWDR26 via inhibiting miR-212-3p. In vivo experiment demonstrated that circWDR26 was essential for EC tumor growth. Conclusion circWDR26 promoted EC progression by regulating miR-212-3p/MSH2 axis and provided novel insights into anti-cancer treatment.
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spelling doaj.art-0d5eee25f1f441f6ac67077f635dc19d2022-12-22T01:33:20ZengBMCEuropean Journal of Medical Research2047-783X2022-07-0127111110.1186/s40001-022-00755-3CircWDR26 regulates endometrial carcinoma progression via miR-212-3p-mediated typing genes MSH2Tao-Xiang Lei0De-Jian He1Jian Cao2Wang-Gui Lv3Department of Gynecological Oncology Surgery, Chenzhou First People’s Hospital (The First Affiliated Hospital of Xiangnan University)Department of Emergency, Chenzhou First People’s Hospital (The First Affiliated Hospital of Xiangnan University)Medical Imaging Center, Chenzhou Fourth People’s HospitalDepartment of Gynecological Oncology Surgery, Chenzhou First People’s Hospital (The First Affiliated Hospital of Xiangnan University)Abstract Background Circular RNAs (circRNA) are important in mediating tumor progression, but their roles in endometrial carcinoma (EC) are not fully understood yet. Many circRNAs are dysregulated and may contribute to EC progression. The functions of circWDR26 in EC remain unknown. Methods The expression of circWDR26 in EC and adjacent normal tissues, and cell lines was determined by qPCR. The proliferation, apoptosis, migration, and invasion of EC cells was examined by CCK-8 assay, flow cytometry, wound healing assay and Transwell assay. The interaction between circWDR26, MSH2 and miR-212-3p was determined by luciferase assay. EC cells were inoculated into nude mice and tumor burden was determined by measuring tumor dimensions, size, and weight. The proliferative marker Ki67 in EC tissue was determined by immunohistochemistry. Results The expression of circWDR26 in EC tissues or cell lines was higher than in the normal tissue or endometrial epithelial cells. Downregulation of circWDR26 resulted in attenuated proliferation, increased apoptosis, reduced migration and invasion of EC cells. Mechanistically, circWDR26 targeted and suppressed the expression of miR-212-3p. We further found that MSH2 was the novel target of miR-212-3p and was upregulated by circWDR26 via inhibiting miR-212-3p. In vivo experiment demonstrated that circWDR26 was essential for EC tumor growth. Conclusion circWDR26 promoted EC progression by regulating miR-212-3p/MSH2 axis and provided novel insights into anti-cancer treatment.https://doi.org/10.1186/s40001-022-00755-3Endometrial carcinomaCircWDR26MiR-212-3pMSH2
spellingShingle Tao-Xiang Lei
De-Jian He
Jian Cao
Wang-Gui Lv
CircWDR26 regulates endometrial carcinoma progression via miR-212-3p-mediated typing genes MSH2
European Journal of Medical Research
Endometrial carcinoma
CircWDR26
MiR-212-3p
MSH2
title CircWDR26 regulates endometrial carcinoma progression via miR-212-3p-mediated typing genes MSH2
title_full CircWDR26 regulates endometrial carcinoma progression via miR-212-3p-mediated typing genes MSH2
title_fullStr CircWDR26 regulates endometrial carcinoma progression via miR-212-3p-mediated typing genes MSH2
title_full_unstemmed CircWDR26 regulates endometrial carcinoma progression via miR-212-3p-mediated typing genes MSH2
title_short CircWDR26 regulates endometrial carcinoma progression via miR-212-3p-mediated typing genes MSH2
title_sort circwdr26 regulates endometrial carcinoma progression via mir 212 3p mediated typing genes msh2
topic Endometrial carcinoma
CircWDR26
MiR-212-3p
MSH2
url https://doi.org/10.1186/s40001-022-00755-3
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AT jiancao circwdr26regulatesendometrialcarcinomaprogressionviamir2123pmediatedtypinggenesmsh2
AT wangguilv circwdr26regulatesendometrialcarcinomaprogressionviamir2123pmediatedtypinggenesmsh2