NDLI: An indolylquinoline derivative promotes apoptosis in human lung cancer cells by impairing mitochondrial functions

Content Provider	Springer Nature Link
Author	Liu, Chun Yen Wu, Pei Tsen Wang, Jing Ping Fan, Po Wei Hsieh, Chang Hung Su, Chun Li Chiu, Chien Chih Yao, Ching Fa Fang, Kang
Copyright Year	2015
Abstract	A number of effective anti-cancer drugs contain either indole or quinoline group. Compounds fused indole and quinoline moieties altogether as indolylquinoline were rarely reported as anti-cancer agents. We reported here that a synthetic indolylquinoline derivative, 3-((7-ethyl-1H-indol-3-yl)-methyl)-2-methylquinoline (EMMQ), inhibited the growth of human non-small cell lung cancer (NSCLC) cells in dose- and time-dependent manners. The cytotoxicity was mediated through apoptotic cell death that began with mitochondrial membrane potential interruption and DNA damage. EMMQ caused transient elevation of p53 that assists in cytochrome c release, cleavage of downstream PARP and procaspase-3 and mitochondria-related apoptosis. The degree of apoptotic cell death depends on the status of tumor suppressor p53 of the target cells. H1299 cells with stable ectopic expression of p53 induced cytotoxicity by disrupting mitochondria functions that differed with those transfected with mutant p53. Knocking-down of p53 attenuated drug effects. EMMQ suppressed the growth of A549 tumor cells in xenograft tumors by exhibiting apoptosis characteristics. Given its small molecular weight acting as an effective p53 regulator in NSCLC cells, EMMQ could be an addition to the current list of lung cancer treatment.
Starting Page	1471
Ending Page	1482
Page Count	12
File Format	PDF
ISSN	13608185
Journal	Apoptosis
Volume Number	20
Issue Number	11
e-ISSN	1573675X
Language	English
Publisher	Springer US
Publisher Date	2015-09-08
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Indolylquinoline Human non-small-cell-lung-cancer cells Apoptosis RNA interference p53 Cancer Research Cell Biology Oncology Biochemistry Virology
Content Type	Text
Resource Type	Article
Subject	Pharmaceutical Science Biochemistry (medical) Cell Biology Clinical Biochemistry Cancer Research Pharmacology

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