Anti-proliferative Effects of Bee Venom through Induction of Bax and Cdk Inhibitor p21WAF1/CIP1 in Human Lung Carcinoma Cells

Bax 및 Cdk inhibitor p21WAF1/CIP1 발현 증가에 의한 bee venom의 A549 인체폐암세포 성장억제

  • Choi, Yung-Hyun (Department of Biochemistry and Biomedical Research Center of Oriental Medicine, Dongeui University College of Oriental Medicine)
  • 최영현 (동의대학교 한의과대학 생화학교실 및 한방바이오연구센타)
  • Published : 2005.02.25

Abstract

To investigate the possible molecular mechanism (s) of bee venom as a candidate of anti-cancer drug, we examined the effects of the compound on the growth of human lung carcinoma cell line A549. Bee venom treatment declined the cell growth and viability of A549 cells in a concentration-dependent manner, which was associated with induction of apoptotic cell death. Bee venom down-regulated the levels of anti-apoptotic genes such as Bcl-2 and Bcl-XS/L, however, the levels of Bax, a pro-apoptotic gene, were up-regulated. Bee venom treatment induced not only tumor suppressor p53 but also cyclin-dependent kinase inhibitor p21WAF1/CIP1 expression in a dose-dependent manner. Furthermore, bee venom treatment induced the down-regulation of telomerase reverse transcriptase mRNA and telomeric repeat binding factor expression of A549 cells, however, the levels of telomerase-associated protein-1 and c-myc were not affected. Taken together, these findings suggest that bee venom-induced inhibition of human lung cancer cell growth is associated with the induction of apoptotic cell death via regulation of several major growth regulatory gene products, and bee venom may have therapeutic potential in human lung cancer.

Keywords

References

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