Actein inhibits cell proliferation and migration and promotes cell apoptosis in human non-small cell lung cancer cells.

Abstract:

:Non-small cell lung cancer (NSCLC) is the leading cause of death in smokers and the most common cause for cancer mortality in both males and females in the United States. Predisposition of this malignancy to distant metastasis leads to poor prognosis; therefore, it is urgent to discover novel therapeutic agents for metastatic NSCLC. The present study aimed to investigate the effects of actein treatment on NSCLC cell growth and migration. Cell viability assays demonstrated that administration of actein markedly inhibited NSCLC cell proliferation in a dose- and time-dependent manner. Transwell assays demonstrated that actein treatment suppressed cell migration and invasion in two NSCLC cell lines, A549 and 95D. Furthermore, treatment with actein remarkably increased the activities of caspase-3 and -9 in NSCLC cells. The protein expression levels of cytoplasmic BCL2 apoptosis regulator (Bcl-2) and BCL2 associated X (Bax) were markedly decreased, while the protein expression levels of mitochondrial Bax, caspase-3, -9 and cytochrome c were upregulated following actein treatment, as evidenced by western blot analysis. The present results demonstrated that actein inhibited cell proliferation and metastasis and promoted cell apoptosis in NSCLC cells, which indicated that actein administration might serve as a potential therapeutic strategy for the treatment of NSCLC in the clinic.

journal_name

Oncol Lett

journal_title

Oncology letters

authors

Zhang Y,Lian J,Wang X

doi

10.3892/ol.2017.7668

subject

Has Abstract

pub_date

2018-03-01 00:00:00

pages

3155-3160

issue

3

eissn

1792-1074

issn

1792-1082

pii

OL-0-0-7668

journal_volume

15

pub_type

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