Open AccessOverexpression of WDR 79 in non‐small cell lung cancer is linked to tumour progression
Author(s) -
Sun Yang,
Yang Chao,
Chen Jieying,
Song Xin,
Li Zhen,
Duan Minlan,
Li Jianglin,
Hu Xiaoxiao,
Wu Kuangpei,
Yan Guobei,
Yang Cai,
Liu Jing,
Tan Weihong,
Ye Mao
Publication year - 2016
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.12759
Subject(s) - cell cycle , cancer research , gene knockdown , carcinogenesis , cell cycle checkpoint , cell growth , telomerase , biology , apoptosis , cyclin b1 , cyclin , cyclin e , cyclin e1 , microbiology and biotechnology , cancer , cyclin dependent kinase 1 , genetics , gene
Abstract WD ‐repeat protein 79 ( WDR 79), a member of the WD ‐repeat protein family, acts as a scaffold protein, participating in telomerase assembly, Cajal body formation and DNA double‐strand break repair. Here, we first report that WDR 79 is frequently overexpressed in cell lines and tissues derived from non‐small cell lung cancer ( NSCLC ). Knockdown of WDR 79 significantly inhibited the proliferation of NSCLC cells in vitro and in vivo by inducing cell cycle arrest and apoptosis. WD‐repeat protein 79 ‐induced cell cycle arrest at the G0/G1 phase was associated with the expression of G0/G1‐related cyclins and cyclin‐dependent kinase complexes. We also provide evidence that WDR 79 knockdown induces apoptosis via a mitochondrial pathway. Collectively, these results suggest that WDR 79 is involved in the tumorigenesis of NSCLC and is a potential novel diagnostic marker and therapeutic target for NSCLC .