miR-218 promoted the apoptosis of human ovarian carcinoma cells via suppression of the WNT/β-catenin signaling pathway
- Authors: Huang Y.1,2, Liang S.1,2, Xiang L.1,2, Han X.1,2, Zhang W.1,2, Tang J.1,2, Wu X.1,2, Zhang M.1,2
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Affiliations:
- Department of Gynecologic Oncology
- Department of Oncology, Shanghai Medical College
- Issue: Vol 51, No 4 (2017)
- Pages: 555-561
- Section: Molecular Cell Biology
- URL: https://journal-vniispk.ru/0026-8933/article/view/163143
- DOI: https://doi.org/10.1134/S0026893317030062
- ID: 163143
Cite item
Abstract
MicroRNA-218 (miR-218) is a short, noncoding RNA, with multiple biological functions. In this study, we aimed to investigate the potential effects of miR-218 on the apoptosis of human ovarian carcinoma cells and the underlying mechanisms by which miR-218 exerted its actions. After over-expressing miR-218 in human ovarian carcinoma (OVCAR3) cells, cell viability was determined by MTT method, cell apoptosis was observed by flow cytometry (FCM), mRNA expression of miR-218, Bcl2, Bax was measured by RT-PCR and protein expression levels of Wnt, tankyrase and β-catenin were quantified by Western blots. Over-expression of miR-218 potently suppressed cell viability and promoted the apoptosis of human ovarian carcinoma cells in a time-dependent manner. In addition, the down-regulation of tankyrase expression level was detected in miR-218-over-expressed cells. Following the block of the Wnt/β-catenin signaling pathway using the inhibitor XAV-939, the effects of miR-218 on the proliferation and apoptosis of human ovarian carcinoma cells were significantly suppressed. Augmenting expression of miR-218 and/or miRNA-218 mimicking therapeutics may provide viable avenue for the treatment of ovarian cancer.
About the authors
Y. Huang
Department of Gynecologic Oncology; Department of Oncology, Shanghai Medical College
Email: hyhuangyan2014@sina.com
China, Shanghai, 200032; Shanghai, 200032
S.-H. Liang
Department of Gynecologic Oncology; Department of Oncology, Shanghai Medical College
Email: hyhuangyan2014@sina.com
China, Shanghai, 200032; Shanghai, 200032
L.-B. Xiang
Department of Gynecologic Oncology; Department of Oncology, Shanghai Medical College
Email: hyhuangyan2014@sina.com
China, Shanghai, 200032; Shanghai, 200032
X.-T. Han
Department of Gynecologic Oncology; Department of Oncology, Shanghai Medical College
Email: hyhuangyan2014@sina.com
China, Shanghai, 200032; Shanghai, 200032
W. Zhang
Department of Gynecologic Oncology; Department of Oncology, Shanghai Medical College
Email: hyhuangyan2014@sina.com
China, Shanghai, 200032; Shanghai, 200032
J. Tang
Department of Gynecologic Oncology; Department of Oncology, Shanghai Medical College
Email: hyhuangyan2014@sina.com
China, Shanghai, 200032; Shanghai, 200032
X.-H. Wu
Department of Gynecologic Oncology; Department of Oncology, Shanghai Medical College
Email: hyhuangyan2014@sina.com
China, Shanghai, 200032; Shanghai, 200032
M.-Q. Zhang
Department of Gynecologic Oncology; Department of Oncology, Shanghai Medical College
Author for correspondence.
Email: hyhuangyan2014@sina.com
China, Shanghai, 200032; Shanghai, 200032
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