Study of Celastrol on Akt Signaling Pathway and Its Roles in the Apoptosis of K562 Cells

HTML  XML Download Download as PDF (Size: 1677KB)  PP. 463-469  
DOI: 10.4236/jct.2011.24062    4,418 Downloads   7,895 Views  Citations

Affiliation(s)

.

ABSTRACT

The purpose Celastrol, the main active compound of the Celastrus genus plants, belonging to Celastraceae, has recently marked antitumour potency on solid tumours of various derivations, Methods: We demonstrate here that Celastrol also present powerful antileukaemic potency through both growth arrest and apoptosis induction in K562 cells, which was accompanied by typical apoptotic morphological and sharp decreased expression of phosphorylation level of Caspase family members and Akt signaling pathway related proteins were determined by western blot before and after celastrol treatment, and further the effect of AKT signaling pathway on celastrol-induced-apoptosis was analyzed. However, in vitro treatment with Celastrol resulted in significantly reduced expression of phophorylation of Akt, Survivin and Bcl-2 significantly in K562 cells. Results: 25 nmol/L WORT (PI3K-Akt inhibitor) can significantly augmented cell apoptosis induced by Celastrol in K562 cells in dose-dependent manner, Moreover, most Caspase3,8,6 were activated in K562 cells during Celastrol treatment, 50 µmol/Lz-VAD-fmk (Caspase inhibitor) can to enhance the apoptosis induced by Celastrol. Discussion: These results suggest that the fact that Akt signaling pathway might act as new targets of Celastrol, correlates well with the sensitivity to Celastrol, as well as the rate of apoptosis induced by Celastrol, Mechanisms that regulate Akt signaling pathway may be provide novel opportunities for drug development.

Share and Cite:

X. Wang, Q. Wu, X. Yang, L. Zhang, Y. Wu and Y. Shu, "Study of Celastrol on Akt Signaling Pathway and Its Roles in the Apoptosis of K562 Cells," Journal of Cancer Therapy, Vol. 2 No. 4, 2011, pp. 463-469. doi: 10.4236/jct.2011.24062.

Copyright © 2024 by authors and Scientific Research Publishing Inc.

Creative Commons License

This work and the related PDF file are licensed under a Creative Commons Attribution 4.0 International License.