Mechanism of α-lipoic acid-induced apoptosis of lung cancer cells: Involvement of Ca2+

Sang Yong Choi, Ji Hoon Yu, Hyeyoung Kim

Research output: Chapter in Book/Report/Conference proceedingConference contribution

25 Citations (Scopus)

Abstract

α-Lipoic acid (LA) shows a protective effect on oxidative stress-induced apoptosis while it induces apoptosis in various cancer cells. Intracellular Ca2+ plays a central role in triggering apoptotic pathways. In the present study, we aim to investigate whether LA induces apoptosis in lung cancer cells and whether Ca2+ is involved in LA-induced apoptosis. We found that LA decreased cell viability and increased DNA fragmentation of the cells. LA activated the caspase-independent pathway, determined by upregulation of poly(ADP-ribose) polymerase (PARP) and increased the nuclear level of apoptosis-inducing factor and caspase-dependent apoptotic pathway, determined by increased levels of cytochrome c and PARP-1 cleavage product. LA-induced apoptotic alterations were inhibited in the cells treated with Ca2+ chelator BAPTA-AM. In conclusion, LA induces apoptosis through caspase-independent and caspase-dependent pathways, which is mediated by intracellular Ca2+.

Original languageEnglish
Title of host publicationNatural Compounds and Their Role in Apoptotic Cell Signaling Pathways
PublisherBlackwell Publishing Inc.
Pages149-155
Number of pages7
ISBN (Print)9781573317375
DOIs
Publication statusPublished - 2009 Aug

Publication series

NameAnnals of the New York Academy of Sciences
Volume1171
ISSN (Print)0077-8923
ISSN (Electronic)1749-6632

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

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    Choi, S. Y., Yu, J. H., & Kim, H. (2009). Mechanism of α-lipoic acid-induced apoptosis of lung cancer cells: Involvement of Ca2+. In Natural Compounds and Their Role in Apoptotic Cell Signaling Pathways (pp. 149-155). (Annals of the New York Academy of Sciences; Vol. 1171). Blackwell Publishing Inc.. https://doi.org/10.1111/j.1749-6632.2009.04708.x