Tags

Type your tag names separated by a space and hit enter

Mechanisms for the magnolol-induced cell death of CGTH W-2 thyroid carcinoma cells.
J Cell Biochem. 2007 Jul 01; 101(4):1011-22.JC

Abstract

Magnolol, a substance purified from the bark of Magnolia officialis, inhibits cell proliferation and induces apoptosis in a variety of cancer cells. The aim of this study was to study the effects of magnolol on CGTH W-2 thyroid carcinoma cells. After 24 h treatment with 80 microM magnolol in serum-containing medium, about 50% of the cells exhibited apoptotic features and 20% necrotic features. Cytochrome-c staining was diffused in the cytoplasm of the apoptotic cells, but restricted to the mitochondria in control cells. Western blot analyses showed an increase in levels of activated caspases (caspase-3 and -7) and of cleaved poly (ADP-ribose) polymerase (PARP) by magnolol. Concomitantly, immunostaining for apoptosis inducing factor (AIF) showed a time-dependent translocation from the mitochondria to the nucleus. Inhibition of either PARP or caspase activity blocked magnolol-induced apoptosis, supporting the involvement of the caspases and PARP. In addition, magnolol activated phosphatase and tensin homolog deleted on chromosome 10 (PTEN) and inactivated Akt by decreasing levels of phosphorylated PTEN and phosphorylated Akt. These data suggest that magnolol promoted apoptosis probably by alleviating the inhibitory effect of Akt on caspase 9. Furthermore, inhibition of PARP activity, but not of caspase activity, completely prevented magnolol-induced necrosis, suggesting the notion that it might be caused by depletion of intracellular ATP levels due to PARP activation. These results show that magnolol initiates apoptosis via the cytochrome-c/caspase 3/PARP/AIF and PTEN/Akt/caspase 9/PARP pathways and necrosis via PARP activation.

Authors+Show Affiliations

Department of Surgery and Division of General Surgery, Far Eastern Memorial Hospital, Taipei, Taiwan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17390340

Citation

Huang, Shih-Horng, et al. "Mechanisms for the Magnolol-induced Cell Death of CGTH W-2 Thyroid Carcinoma Cells." Journal of Cellular Biochemistry, vol. 101, no. 4, 2007, pp. 1011-22.
Huang SH, Chen Y, Tung PY, et al. Mechanisms for the magnolol-induced cell death of CGTH W-2 thyroid carcinoma cells. J Cell Biochem. 2007;101(4):1011-22.
Huang, S. H., Chen, Y., Tung, P. Y., Wu, J. C., Chen, K. H., Wu, J. M., & Wang, S. M. (2007). Mechanisms for the magnolol-induced cell death of CGTH W-2 thyroid carcinoma cells. Journal of Cellular Biochemistry, 101(4), 1011-22.
Huang SH, et al. Mechanisms for the Magnolol-induced Cell Death of CGTH W-2 Thyroid Carcinoma Cells. J Cell Biochem. 2007 Jul 1;101(4):1011-22. PubMed PMID: 17390340.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Mechanisms for the magnolol-induced cell death of CGTH W-2 thyroid carcinoma cells. AU - Huang,Shih-Horng, AU - Chen,Ying, AU - Tung,Po-Yuan, AU - Wu,Jiahn-Chun, AU - Chen,Kuo-Hsin, AU - Wu,Jiann-Ming, AU - Wang,Seu-Mei, PY - 2007/3/29/pubmed PY - 2007/9/12/medline PY - 2007/3/29/entrez SP - 1011 EP - 22 JF - Journal of cellular biochemistry JO - J. Cell. Biochem. VL - 101 IS - 4 N2 - Magnolol, a substance purified from the bark of Magnolia officialis, inhibits cell proliferation and induces apoptosis in a variety of cancer cells. The aim of this study was to study the effects of magnolol on CGTH W-2 thyroid carcinoma cells. After 24 h treatment with 80 microM magnolol in serum-containing medium, about 50% of the cells exhibited apoptotic features and 20% necrotic features. Cytochrome-c staining was diffused in the cytoplasm of the apoptotic cells, but restricted to the mitochondria in control cells. Western blot analyses showed an increase in levels of activated caspases (caspase-3 and -7) and of cleaved poly (ADP-ribose) polymerase (PARP) by magnolol. Concomitantly, immunostaining for apoptosis inducing factor (AIF) showed a time-dependent translocation from the mitochondria to the nucleus. Inhibition of either PARP or caspase activity blocked magnolol-induced apoptosis, supporting the involvement of the caspases and PARP. In addition, magnolol activated phosphatase and tensin homolog deleted on chromosome 10 (PTEN) and inactivated Akt by decreasing levels of phosphorylated PTEN and phosphorylated Akt. These data suggest that magnolol promoted apoptosis probably by alleviating the inhibitory effect of Akt on caspase 9. Furthermore, inhibition of PARP activity, but not of caspase activity, completely prevented magnolol-induced necrosis, suggesting the notion that it might be caused by depletion of intracellular ATP levels due to PARP activation. These results show that magnolol initiates apoptosis via the cytochrome-c/caspase 3/PARP/AIF and PTEN/Akt/caspase 9/PARP pathways and necrosis via PARP activation. SN - 0730-2312 UR - https://www.unboundmedicine.com/medline/citation/17390340/Mechanisms_for_the_magnolol_induced_cell_death_of_CGTH_W_2_thyroid_carcinoma_cells_ L2 - https://doi.org/10.1002/jcb.21100 DB - PRIME DP - Unbound Medicine ER -