The overexpression of KIFC1 was associated with the proliferation and prognosis of non-small cell lung cancer

被引:34
|
作者
Liu, Yafang [1 ]
Zhan, Ping [2 ]
Zhou, Zejun [1 ]
Xing, Ze [2 ]
Zhu, Suhua [1 ]
Ma, Chenhui [1 ]
Li, Qian [1 ]
Zhu, Qingqing [1 ]
Miao, Yingying [1 ]
Zhang, Jianya [1 ]
Lv, Tangfeng [1 ,2 ]
Song, Yong [1 ,2 ]
机构
[1] Southern Med Univ, Jinling Hosp, Dept Resp Med, 305 East Zhongshan Rd, Nanjing 210002, Jiangsu, Peoples R China
[2] Nanjing Univ, Sch Med, Jinling Hosp, Dept Resp Med, Nanjing 210002, Jiangsu, Peoples R China
基金
中国国家自然科学基金;
关键词
Kinesin family member C1 (KIFC1); non-small cell lung cancer (NSCLC); cyclin-dependent kinase inhibitor 1A (p21); cell division cycle protein 2 homolog (cdc2); prognostic; TUMOR PROGRESSION; CYCLE ARREST; PROTEIN; EXPRESSION; APOPTOSIS; NETWORKS; MITOSIS; GROWTH; GENES; CHINA;
D O I
10.21037/jtd.2016.10.67
中图分类号
R56 [呼吸系及胸部疾病];
学科分类号
摘要
Background: The kinesin family member C1 (KIFC1, also known as HSET) is a kinesin superfamily protein (KIFs). Although KIFC1 acts as a crucial role in the development of several human cancers, the KIFC1 expression profile and functional remain unclear in non-small cell lung cancer (NSCLC). Methods: We collected the fresh NSCLC samples and paired normal lung tissue in patients with lung cancer operation, and detected KIFC1 expression using quantitative reverse-transcription polymerase chain reaction (qRT-PCR) and Western blotting. To expand on previous smaller-scale studies, NSCLC tissue microarrays (TMA) were analyzed by IHC. Finally, cell lines were employed to further probe the potential mechanisms, Results: In this study, we described that KIFC1 was significantly upregulated in NSCLC tissues compared with the corresponding normal tissues. Moreover, KIFC1 overexpression was associated with the poor overall survival (OS) of NSCLC patients, and siRNA-mediated knockdown of KIFC1 significantly suppressed tumor cell proliferation in vitro. Further verification showed that inhibition of KIFC1 gene expression caused the upregulation of the cyclin-dependent kinases inhibitor p21 and downregulation of the cell cycle driver protein cdc2, which arrested cells in the G2-M phase. Conclusions: we report that increased KIFC1 expression may promote cell proliferation and identified it as a biomarker of unfavorable prognosis in NSCLC patients.
引用
收藏
页码:2911 / 2923
页数:13
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