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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
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