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MicroRNA-205 inhibits the proliferation and invasion of breast cancer by regulating AMOT expression
Author(s) -
Haige Zhang,
Qing-xia Fan
Publication year - 2015
Publication title -
oncology reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.094
H-Index - 96
eISSN - 1791-2431
pISSN - 1021-335X
DOI - 10.3892/or.2015.4148
Subject(s) - oncogene , gene knockdown , cancer research , carcinogenesis , microrna , downregulation and upregulation , molecular medicine , biology , breast cancer , cancer , cell cycle , cell growth , small interfering rna , mcf 7 , apoptosis , transfection , cell culture , gene , human breast , genetics
It has been reported that the expression of angiomotin (AMOT) is upregulated in breast cancer. However, the regulatory mechanism remains unknown. In the present study, we aimed to ascertain whether the expression of AMOT is regulated by microRNAs (miRNAs) in breast cancer. In the present study, miR-205 was significantly downregulated in breast cancer samples and it was identified to directly target the 3'-untranslated region (3'-UTR) of AMOT in breast cancer MCF-7 cells by luciferase assay. miR-205 and small interfering RNA (siRNA)-mediated AMOT-knockdown experiments revealed that miR-205 significantly inhibited the proliferation and the invasion of MCF-7 cells through a decrease in the expression of AMOT, yet had no effect on apoptosis. Furthermore, we observed that the overexpression of AMOT partially reversed the inhibitory effect of miR-205 on the growth and the invasion of MCF-7 cells. The data indicated that miR-205 regulated the proliferation and the invasion of breast cancer cells through suppression of AMOT expression, at least partly. Therefore, the disordered decreased expression of miR-205 and the resulting AMOT upregulation contributes to breast carcinogenesis, and miR-205-AMOT represents a new potential therapeutic target for the treatment of breast carcinoma.

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