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Article Publish Status: FREE
Abstract Title:

Panaxydol Derived from Panax ginseng Inhibits GCell Cycle Progression in Non-small Cell Lung Cancer via Upregulation of Intracellular CaLevels.

Abstract Source:

Biol Pharm Bull. 2018 ;41(11):1701-1707. PMID: 30381670

Abstract Author(s):

Jeong-Hun Lee, Dong Gyu Leem, Kyung-Sook Chung, Kyung-Tack Kim, Sang Yoon Choi, Kyung-Tae Lee

Article Affiliation:

Jeong-Hun Lee

Abstract:

Panaxydol, a polyacetylenic compound derived from Panax ginseng has been reported to suppress the growth of cancer cells. However, the molecular mechanisms underlying cell cycle arrest by this compound in non-small cell lung cancer (NSCLC) are unknown. Our study found that panaxydol treatment induced cell cycle arrest at Gphase in NSCLC cells. The cell cycle arrest was accompanied by down-regulation of the protein expression of cyclin-dependent kinase (CDK) 2, CDK4, CDK6, cyclin Dand cyclin E, and decrease in the phosphorylation of retinoblastoma (Rb) protein. Furthermore, up-regulation of cyclin-dependent kinase inhibitor (CDKI) p21and p27was observed in panaxydol-treated NSCLC cells. In addition, panaxydol also induced accumulation of intracellular Ca([Ca]). (Acetyloxy)methyl 2-({2-[(acetyloxy)methoxy]-2-oxoethyl}[2-(2-{2-[bis({2-[(acetyloxy)methoxy]-2-oxoethyl})amino]phenoxy}ethoxy)phenyl]amino)acetate (BAPTA-AM), the Cachelator, attenuated not only panaxydol-induced accumulation of [Ca], but also Gcell cycle arrest and decrease of CDK6 and cyclin Dprotein expression level. These results demonstrated that the anti-proliferative effects of panaxydol were caused by cell cycle arrest, which is closely linked to the up-regulation of [Ca]and represents a promising approach for the treatment of lung cancer.

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