详细信息

Jinfukang induces cellular apoptosis through activation of Fas and DR4 in A549 cells  ( SCI-EXPANDED收录)  

文献类型:期刊文献

英文题名:Jinfukang induces cellular apoptosis through activation of Fas and DR4 in A549 cells

作者:Lu, Jun[1,2];Chen, Jian[1,2];Kang, Yani[1,2,3];Wu, Jun[1,2];Shi, Hui[4];Fu, Yanli[5];Jiao, Lijing[3];Dong, Changsheng[3];Li, Xiaowei[1,2];Jin, Yu[4];Zhao, Wei[6];Xu, Ling[3,7];Zhao, Xiaodong[1,2,3]

机构:[1]Shanghai Jiao Tong Univ, Shanghai Ctr Syst Biomed, Sch Biomed Engn, 800 Dongchuan Rd, Shanghai 200240, Peoples R China;[2]Shanghai Jiao Tong Univ, BioID Ctr, 800 Dongchuan Rd, Shanghai 200240, Peoples R China;[3]Shanghai Univ Tradit Chinese Med, Tumor Inst Tradit Chinese Med, Longhua Hosp, Shanghai 200032, Peoples R China;[4]East China Univ Sci & Technol, Engn Res Ctr Pharmaceut Proc Chem, Minist Educ, Sch Pharm, Shanghai 200237, Peoples R China;[5]Xinjiang Med Univ, Dept Oncol, Affiliated Hosp 4, Urumqi 830000, Xinjiang, Peoples R China;[6]Shanghai Jiao Tong Univ, Sch Med, Lab Microbiol & Parasitol, Expt Teaching Ctr, Shanghai 200025, Peoples R China;[7]Shanghai Univ Tradit Chinese Med, Dept Oncol, Yueyang Hosp Integrated Tradit Chinese & Western, Shanghai 200437, Peoples R China

年份:2018

卷号:16

期号:4

起止页码:4343

外文期刊名:ONCOLOGY LETTERS

收录:;WOS:【SCI-EXPANDED(收录号:WOS:000444990700033)】;

基金:The authors would like to thank Professor Daniel M. Czajkowsky (School of Biomedical Engineering and Bio-ID Center, Shanghai Jiao Tong University, Shanghai, China) for helpful discussion and careful proofreading. The present study was supported by Longhua Medical Project of State Clinical Research Center of TCM in Longhua Hospital (grant nos. LYTD-21 and JDZX2012123), National Basic Research Program of China (grant no. 2013CB967402) and National Natural Science Foundation of China (grant nos. 81373623 and 91229123).

语种:英文

外文关键词:Jinfukang formula; traditional Chinese medicine; apoptosis; cell cycle arrest; non-small cell lung cancer; transcriptome

摘要:The traditional Chinese medicine Jinfukang (JFK) has been shown as a valuable drug to treat non-small cell lung cancer (NSCLC). Previously, it was reported that JFK-induced epigenetic alteration is involved in anti-lung cancer activity. In the present study, the effect of JFK on lung cancer cell lines was examined with the aim to further understand the underlying mechanisms of JFK-induced anti-lung cancer activity by transcriptome profiling analysis. JFK was observed to decrease lung cancer cell viability and simultaneously induce cellular morphology alteration. Additionally, this causes cell cycle arrest and apoptosis in A549 cells. The present RNA-seq analysis identified 5,281 genes with differential expression (P<0.05). Gene ontology analysis indicated that genes involved in the cell cycle pathway are downregulated, including cyclin-dependent kinase 2, cyclin-dependent kinase 4, cyclin B1 and cyclin A2, and apoptosis-associated genes are upregulated, including Fas, death receptor 4 (DR4), tumor protein P53 binding protein 2 and BCL2 interacting protein 3 like. Particularly, the present results indicate knockdown of Fas and DR4 attenuates JFK-induced apoptosis in A549 cells. Overall, the present study suggests JFK induces cellular apoptosis through activation of Fas and DR4 in A549 cells and provides an insight for understanding the antitumor mechanisms of this Chinese traditional medicine.

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