Lu Jun, Chen Jian, Kang Yani, Wu Jun, Shi Hui, Fu Yanli, Jiao Lijing, Dong Changsheng, Li Xiaowei, Jin Yu, Zhao Wei, Xu Ling, Zhao Xiaodong
Shanghai Center for Systems Biomedicine, School of Biomedical Engineering and Bio-ID Center, Shanghai Jiao Tong University, Shanghai 200240, P.R. China.
Tumor Institute of Traditional Chinese Medicine, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, P.R. China.
Oncol Lett. 2018 Oct;16(4):4343-4352. doi: 10.3892/ol.2018.9149. Epub 2018 Jul 16.
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 , death receptor 4 (), tumor protein P53 binding protein 2 and BCL2 interacting protein 3 like. Particularly, the present results indicate knockdown of and attenuates JFK-induced apoptosis in A549 cells. Overall, the present study suggests JFK induces cellular apoptosis through activation of and in A549 cells and provides an insight for understanding the antitumor mechanisms of this Chinese traditional medicine.
中药金复康（JFK）已被证明是治疗非小细胞肺癌（NSCLC）的一种有价值的药物。此前有报道称，JFK诱导的表观遗传改变与抗肺癌活性有关。在本研究中，通过转录组分析来检测JFK对肺癌细胞系的作用，以进一步了解JFK诱导抗肺癌活性的潜在机制。观察到JFK可降低肺癌细胞活力，并同时诱导细胞形态改变。此外，这会导致A549细胞的细胞周期停滞和凋亡。目前的RNA测序分析鉴定出5281个差异表达基因（P<0.05）。基因本体分析表明，参与细胞周期途径的基因被下调，包括细胞周期蛋白依赖性激酶2、细胞周期蛋白依赖性激酶4、细胞周期蛋白B1和细胞周期蛋白A2，而与凋亡相关的基因被上调，包括死亡受体4、肿瘤蛋白P53结合蛋白2和BCL2相互作用蛋白3样蛋白。特别地，目前的结果表明敲低和会减弱JFK诱导的A549细胞凋亡。总体而言，本研究表明JFK通过激活A549细胞中的和诱导细胞凋亡，并为理解这种中药的抗肿瘤机制提供了见解。
