z-logo
open-access-imgOpen Access
MicroRNA-29a inhibits cell migration and invasion by targeting Roundabout 1 in breast cancer cells
Author(s) -
Hui Li,
Jiashun Luo,
Bin Xu,
Kongjia Luo,
Juan Hou
Publication year - 2015
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2015.3749
Subject(s) - microrna , oncogene , cancer research , biology , breast cancer , cancer , cell migration , cell , cancer cell , downregulation and upregulation , cell cycle , gene , genetics
Epithelial ovarian cancer (EOC) remains a major gynecological problem, with a poor 5-year-survival rate due to distant metastases. The identification of microRNAs (miRNAs) may provide a novel avenue for diagnostic and treatment regimens for EOC. Several miRNAs have been reported to be involved in the progression of EOC, among which miRNA (miR)-137 has been observed to be downregulated in the ovarian tissues of patients with EOC. However, the functions of miR-137 in EOC cell apoptosis, migration and invasion remain to be elucidated. In the present study, the expression of miR-137 was measured in clinical ovarian cancer specimens and cell lines using reverse transcription-quantitative polymerase chain reaction. The role of miR-137 in the growth and survival of the SKOV3 human ovarian cancer cell line was determined using several in vitro approaches and in nude mouse models. The results demonstrated that the expression of miR-137 was downregulated in the ovarian cancer specimens and cell lines. It was also observed that enforced expression of miR-137 in the EOC cell lines decreased cell proliferation, clonogenicity, migration and invasion, and induced G1 arrest and cell apoptosis in vitro. Notably, the enforced expression of miR-137 suppressed tumor growth in the nude mice models. These findings suggested that miR-137 may act as a tumor suppressor and be used as a potential therapeutic agent for the treatment of EOC.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here