Gang Huang1, Jinliang Yang1, Like Zhang1, Lijuan Cao1, Meng Zhang1, Xiaoguang Niu1, Zhigang Zhou1, Xin Zhang1, Pu Li1, Jun Feng Liu2. 1. Department of Thoracic Surgery, The 3rdHospital of HeBei Medical University, NO.139, Zi Qiang Road, Shi Jia Zhuang, HeBei, 050051, China. 2. Department of Thoracic Surgery, The 4thHospital of HeBei Medical University, NO.12, Jian Kang Road, Shi Jia Zhuang, HeBei, 050011, China. Electronic address: junfeng_liu_4th@163.com.
Abstract
BACKGROUND: The anti-lung tumor potential of 11-carbonyl-β-boswellic acid was investigated. MATERIALS & METHODS: The inhibitory effects of 11-carbonyl-β-boswellic acid on non-small cell lung cancer (NSCLC) was assessed by proliferation, apoptosis, cell cycle and molecular mechanisms in NSCLC H446 cells in vitro. The results showed that the growth of H446 cells was significantly inhibited by 11-carbonyl-β-boswellic acid in a dose- and time-dependent manner. Meanwhile, 11-carbonyl-β-boswellic acid induced cell apoptosis and cell cycle G2-M phase arrest in H446 cells. RESULTS: Mechanistically, 11-carbonyl-β-boswellic acid could activate JNK signaling pathway, down-regulate the expression of surviving protein, and activate the cleavage of PARP, leading to marked inhibitory effect on H446 cells. CONCLUSIONS: These findings suggest that 11-carbonyl-β-boswellic acid may be a potential usefulness for preventing and treatment of NSCLC.
BACKGROUND: The anti-lung tumor potential of 11-carbonyl-β-boswellic acid was investigated. MATERIALS & METHODS: The inhibitory effects of 11-carbonyl-β-boswellic acid on non-small cell lung cancer (NSCLC) was assessed by proliferation, apoptosis, cell cycle and molecular mechanisms in NSCLC H446 cells in vitro. The results showed that the growth of H446 cells was significantly inhibited by 11-carbonyl-β-boswellic acid in a dose- and time-dependent manner. Meanwhile, 11-carbonyl-β-boswellic acid induced cell apoptosis and cell cycle G2-M phase arrest in H446 cells. RESULTS: Mechanistically, 11-carbonyl-β-boswellic acid could activate JNK signaling pathway, down-regulate the expression of surviving protein, and activate the cleavage of PARP, leading to marked inhibitory effect on H446 cells. CONCLUSIONS: These findings suggest that 11-carbonyl-β-boswellic acid may be a potential usefulness for preventing and treatment of NSCLC.