Open AccessSTIP overexpression confers oncogenic potential to human non‐small cell lung cancer cells by regulating cell cycle and apoptosis
Author(s) -
Tang Yani,
Yan Guobei,
Song Xin,
Wu Kuangpei,
Li Zhen,
Yang Chao,
Deng Tanggang,
Sun Yang,
Hu Xiaoxiao,
Yang Cai,
Bai Huarong,
Li Hui,
Tan Weihong,
Ye Mao,
Liu Jing
Publication year - 2015
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.12670
Subject(s) - cell cycle , apoptosis , wnt signaling pathway , mapk/erk pathway , microbiology and biotechnology , kinase , cell growth , cell cycle checkpoint , cyclin a , biology , cyclin dependent kinase 1 , cyclin dependent kinase , protein kinase b , cancer research , gene knockdown , chemistry , signal transduction , biochemistry
Sip1/tuftelin‐interacting protein ( STIP ), a multidomain nuclear protein, is a novel factor associated with the spliceosome, yet its role and molecular function in cancer remain unknown. In this study, we show, for the first time, that STIP is overexpressed in non‐small cell lung cancer ( NSCLC ) tissues compared to adjacent normal lung tissues. The depletion of endogenous STIP inhibited NSCLC cell proliferation in vitro and in vivo , caused cell cycle arrest and induced apoptosis. Cell cycle arrest at the G2/M phase was associated with the expression and activity of the cyclin B1‐ CDK 1 (cyclin‐dependent kinase 1) complex. We also provide evidence that STIP knockdown induced apoptosis by activating both caspase‐9 and caspase‐3 and by altering the Bcl‐2/Bax expression ratio. RNA sequencing data indicated that the MAPK mitogen‐activated protein kinases, Wnt, PI 3K/ AKT , and NF ‐κB (nuclear factor kappa‐light‐chain‐enhancer of activated B cells) signalling pathways might be involved in STIP ‐mediated tumour regulation. Collectively, these results suggest that STIP may be a novel potential diagnostic and therapeutic target for NSCLC .