文献类型：期刊文献

英文题名：ZFX knockdown inhibits growth and migration of non-small cell lung carcinoma cell line H1299

作者：Li, Kui[1,2];Zhu, Zhi-Chuan[1];Liu, Yong-Jie[1];Liu, Ji-Wei[1];Wang, Hong-Tao[1];Xiong, Zhi-Qi[1];Shen, Xu[2];Hu, Ze-Lan[1];Zheng, Jing[1]

机构：[1]E China Univ Sci & Technol, Shanghai Key Lab New Drug Design, Sch Pharm, Shanghai 200237, Peoples R China;[2]Chinese Acad Sci, Shanghai Inst Mat Med, Shanghai 200031, Peoples R China

年份：2013

卷号：6

期号：11

起止页码：2460

外文期刊名：INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000328889300021)】；

基金：This work was supported by the China Post-doctoral Science Special Foundation (2010-03259) to Jing Zheng, and by the Shanghai Committee of Science and Technology (Grant 11DZ2260600).

语种：英文

外文关键词：ZFX; non-small cell lung carcinoma; growth; migration; senescence

摘要：ZFX (zinc finger transcription factor, X chromosome-linked) contributes to the maintenance of different types of stem cells and the progression of various cancers. We have previously reported that ZFX knockdown inhibits proliferation of glioma in vitro and in vivo. Since overexpression of ZFX in lung cancer tissue correlates with lymph node metastasis, we hypothesized that ZFX may play a role in lung cancer. In this study, we identified ZFX as a promoter of lung cancer growth and migration in a NSCLC (non-small cell lung carcinoma) cell line H1299. ZFX knockdown caused proliferation inhibition determined by MTT assay and colony formation assay, G0/G1 arrest of cell cycle and slightly increased proportion of apoptotic cells assessed by flow cytometry assay, decreased population of migrating cells showed by wound-healing assay, increased cell senescence evidenced by senescence-associated beta-galactosidase staining. ZFX knockdown also led to decreased proportion of tumor bearing mice and reduced mean tumor volume in a subcutaneous tumor model. In addition, western blot showed that ZFX knockdown down regulated a set of proteins involved in proliferation, survival and motility. Altogether, these results suggest that ZFX may be a potential therapeutic target for NSCLC.