Upregulation of Limk1 caused by microRNA-138 loss aggravates the metastasis of ovarian cancer by activation of Limk1/cofilin signaling
Author(s) -
Puxiang Chen,
MENGJUN ZENG,
Yan Zhao,
Xiaolin Fang
Publication year - 2014
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.2014.3461
Subject(s) - metastasis , cancer research , microrna , ovarian cancer , oncogene , gene silencing , cancer , cofilin , biology , cell growth , downregulation and upregulation , cell , cell cycle , actin cytoskeleton , genetics , gene , cytoskeleton
LIM kinase 1 (Limk1) is associated with cell prolife-ration and metastasis and its dysregulated expression has been observed in many types of cancer. The present study aimed to examine the role of Limk1 in the development of ovarian cancer, as well as the underlying molecular mechanism involved. The results showed that increased Limk1 and decreased miR-138 expression co-existed in ovarian cancer. Furthermore, knockout of Limk1 or the overexpression of miR-138 resulted in reduced cell invasion and migration, while silencing of miR-138 led to enhancement of the invasion and migration of ovarian cancer cells. Cell growth was inhibited by the overexpression of miR-138, although not by the knockout of Limk1. miR-138 directly targeted Limk1 and inhibited ovarian cancer cell growth by PCNA and Bcl-2. Moreover, Limk1/cofilin/p-cofilin is likely a critical signaling pathway involving in miR-138 modulation of ovarian cancer cell metastasis. The results provide evidence supporting miR-138/Limk1 as a novel diagnostic or therapeutic target for ovarian cancer.
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