已发表论文

MicroRNA 302b-3p/302c-3p/302d-3p 抑制人子宫内膜癌细胞上皮 - 间质转化并促进细胞凋亡

 

Authors Li Y, Huo J, Pan X, Wang C, Ma X

Received 19 October 2017

Accepted for publication 6 December 2017

Published 6 March 2018 Volume 2018:11 Pages 1275—1284

DOI https://doi.org/10.2147/OTT.S154517

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Manfred Beleut

Peer reviewer comments 2

Editor who approved publication: Dr Ingrid Espinoza

Background: Studies have shown that the microRNA miR-302 can affect the proliferation, migration and cell cycle progression of endometrial carcinoma (EC). miR-302 clusters have been shown to play an important role in the proliferation and differentiation of cancer cells and in their tumorigenicity.
Subjects and methods: In this study, we detected the expression of genes through quantitative reverse transcription polymerase chain reaction (qRT-PCR). We detected the expression of proteins through Western blot. The Annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) double-staining assay were used to detect the ability of miR-302b-3p/302c-3p/302d-3p to affect the cell apoptosis. The CCK-8 were used to detect the ability of miR-302b-3p/302c-3p/
302d-3p to affect the cell proliferation. The Cell cycle analysis were used to detect the ability of miR-302b-3p/302c-3p/302d-3p to affect the cell cycle. Finally, the wound healing assay was used to detect the ability of miR-302b-3p/302c-3p/302d-3p to impact cell migration.
Results: We found that miR-302b-3p/302c-3p/302d-3p of the miR-302 cluster was downregulated in EC, and it altered the epithelial–mesenchymal transition (EMT) process in the EC cell lines Ishikawa and HEC-1A. Western blot and the Annexin V- FITC/PI double-staining assay were used to detect the ability of miR-302b-3p/302c-3p/302d-3p to promote the apoptosis of Ishikawa and HEC-1A cells. In addition, qRT-PCR results showed that overexpression of miR-302b-3p/302c-3p/302d-3p significantly inhibited the expression of ZEB1, suppressed the expression of Bcl-2 and promoted the expression of BAX. The overexpression of miR-302b-3p/302c-3p/302d-3p inhibited the proliferation and migration of Ishikawa and HEC-1A cells. Cell cycle analysis showed that miR-302b-3p/302c-3p/302d-3p arrested cell cycle progression in the G0/G1 phase.
Conclusion: All results showed that miR-302b-3p/302c-3p/302d-3p can be used as a tumor suppressor in EC and is expected to be a new target for the treatment of EC.
Keywords: endometrial carcinoma, miR-302b-3p, miR-302c-3p, miR-302d-3p, EMT, cell apoptosis


* 在1278页,1A图表中的y轴标签被错误地列出,标签必须显示为:

 

请点击这里查看详细更正启事