Open AccessFoxO6 inhibits cell proliferation in lung carcinoma through up-regulation of USP7
Author(s) -
Hong-Jun Hu,
Liguo Zhang,
Zhenhua Wang,
Xixi Guo
Publication year - 2012
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.2015.3362
Subject(s) - cell growth , a549 cell , lung cancer , cancer research , biology , cell cycle , gene knockdown , oncogene , ectopic expression , cell , microbiology and biotechnology , cell culture , apoptosis , medicine , pathology , biochemistry , genetics
Emerging evidence has suggested that misregulation of oncogenes and/or tumor suppressors has a crucial role in the development of lung carcinoma. The present study demonstrated that the expression levels of forkhead box O6 (FOXO6) were downregulated in lung cancer tissue samples, as compared with those in adjacent normal tissue. Overexpression of FOXO6 inhibited the proliferation of A549 human lung cancer cells, whereas knockdown of endogenous FOXO6 expression enhanced cell proliferation. Furthermore, ectopic FOXO6 expression induced the expression of ubiquitin-specific-processing protease 7 (USP7). As a result of this regulation, FOXO6 overexpression led to an elevation of p53 protein expression levels in A549 cells. In conclusion, the results of the present study indicated that the FOXO6/USP7 molecular network has an important role in the regulation of lung cancer development.