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HERO ID
4106419
Reference Type
Journal Article
Title
MiR-34a suppresses ovarian cancer proliferation and motility by targeting AXL
Author(s)
Li, R; Shi, X; Ling, F; Wang, C; Liu, J; Wang, W; Li, M
Year
2015
Is Peer Reviewed?
1
Journal
Tumor Biology
ISSN:
1010-4283
EISSN:
1423-0380
Volume
36
Issue
9
Page Numbers
7277-7283
Language
English
PMID
25895459
DOI
10.1007/s13277-015-3445-8
Web of Science Id
WOS:000365033100078
Relationship(s)
has retraction
4098513
Retraction Note to multiple articles in Tumor Biology
Abstract
Increasing evidence has suggested that dysregulation of microRNAs (miRNAs) could contribute to tumor progression. The miR-34 family is directly transactivated by tumor suppressor p53 which is frequently mutated in various cancers; however, the effect of miR-34a on the ovarian cancer cells remains unclear. The aim of the paper was to study the expression of miR-34a in ovarian cancer and miR-34a's relation to the cell proliferation and metastasis in ovarian cancer in vitro. miR-34a expression was determined by quantitative RT-PCR in a panel of 60 human ovarian cancer samples. Functional characterization of miR-34a was accomplished by reconstitution of miR-34a expression in ovarian cancer cells by determining changes in proliferation, migration, and invasion. Our results showed that miR-34a is downregulated in ovarian cancer tissues compared with the corresponding adjacent non-neoplastic tissues, and the expression level of miR-34a was significantly lower in ovarian cancer cell lines in comparison with normal human fallopian tube epithelial cell line. The 3-(4,5)-dimethylthiahiazo(-z-y1)-3,5-diphenytetrazoliumromide (MTT) assay revealed significant cell proliferation inhibition in miR-34a transfectant compared with the control from HO8910 and SKOV3 cells, which displayed lowest expressions of miR-34a. Furthermore, the transwell assay also showed significant cell migration inhibition in miR-34a transfectant, compared with cell lines transfected with NC. Overexpression of miR-34a led to the inhibition of AXL expression, indicating that AXL is a target gene for miR-34a. Our data suggest that miR-34a may function as a tumor suppressor through repression of oncogenic AXL in ovarian cancer.
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