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Influence of Bax or Bcl-2 overexpression on the ceramide-dependent apoptotic pathway in glioma cells.
Oncogene. 2000 Jul 20; 19(31):3508-20.O

Abstract

Ceramide has recently been regarded as a potential mediator of apoptosis. In the present study, the effects of Bcl-2 and Bax on the ceramide-mediated apoptotic pathways were examined in glioma cells overexpressing Bcl-2 or Bax. Etoposide, cisplatin and tumor necrosis factor-alpha induced apoptosis of C6 rat glioma cells which was associated with ceramide formation due to activation of neutral sphingomyelinase, followed by release of mitochondrial cytochrome c into the cytosol and activation of caspases-9 and -3. The growth of C6 cells stably overexpressing either Bcl-2 or Bax was almost equal to that of the vector-transfected cells. Bax overexpression enhanced etoposide-induced apoptosis through acceleration of cytochrome c release and caspases activation. However, Bax had no effect on ceramide formation. Similar findings were obtained in C6 cells and U87-MG human glioblastoma cells which were transiently overexpressed with Bax. In contrast, Bcl-2 overexpression resulted in a retardation of the apoptotic process via prevention of cytochrome c release and caspases activation, and ceramide formation was also blocked when Bcl-2 was highly overexpressed in glioma cells. In addition, transient overexpression of Bcl-xL also exerted inhibitory effects on ceramide formation and apoptotic cell death induced by etoposide. These results indicate that Bax promotes apoptosis regardless of ceramide formation and that Bcl-2 or Bcl-xL prevents ceramide formation by repressing neutral sphingomyelinase as well as ceramide-induced cytochrome c release. Oncogene (2000) 19, 3508 - 3520

Authors+Show Affiliations

Department of Neurosurgery, Gifu University School of Medicine, Tsukasamachi-40, Gifu 500-8705, Japan.No affiliation info availableNo affiliation info availableNo 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

10918609

Citation

Sawada, M, et al. "Influence of Bax or Bcl-2 Overexpression On the Ceramide-dependent Apoptotic Pathway in Glioma Cells." Oncogene, vol. 19, no. 31, 2000, pp. 3508-20.
Sawada M, Nakashima S, Banno Y, et al. Influence of Bax or Bcl-2 overexpression on the ceramide-dependent apoptotic pathway in glioma cells. Oncogene. 2000;19(31):3508-20.
Sawada, M., Nakashima, S., Banno, Y., Yamakawa, H., Takenaka, K., Shinoda, J., Nishimura, Y., Sakai, N., & Nozawa, Y. (2000). Influence of Bax or Bcl-2 overexpression on the ceramide-dependent apoptotic pathway in glioma cells. Oncogene, 19(31), 3508-20.
Sawada M, et al. Influence of Bax or Bcl-2 Overexpression On the Ceramide-dependent Apoptotic Pathway in Glioma Cells. Oncogene. 2000 Jul 20;19(31):3508-20. PubMed PMID: 10918609.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Influence of Bax or Bcl-2 overexpression on the ceramide-dependent apoptotic pathway in glioma cells. AU - Sawada,M, AU - Nakashima,S, AU - Banno,Y, AU - Yamakawa,H, AU - Takenaka,K, AU - Shinoda,J, AU - Nishimura,Y, AU - Sakai,N, AU - Nozawa,Y, PY - 2000/8/3/pubmed PY - 2000/8/29/medline PY - 2000/8/3/entrez SP - 3508 EP - 20 JF - Oncogene JO - Oncogene VL - 19 IS - 31 N2 - Ceramide has recently been regarded as a potential mediator of apoptosis. In the present study, the effects of Bcl-2 and Bax on the ceramide-mediated apoptotic pathways were examined in glioma cells overexpressing Bcl-2 or Bax. Etoposide, cisplatin and tumor necrosis factor-alpha induced apoptosis of C6 rat glioma cells which was associated with ceramide formation due to activation of neutral sphingomyelinase, followed by release of mitochondrial cytochrome c into the cytosol and activation of caspases-9 and -3. The growth of C6 cells stably overexpressing either Bcl-2 or Bax was almost equal to that of the vector-transfected cells. Bax overexpression enhanced etoposide-induced apoptosis through acceleration of cytochrome c release and caspases activation. However, Bax had no effect on ceramide formation. Similar findings were obtained in C6 cells and U87-MG human glioblastoma cells which were transiently overexpressed with Bax. In contrast, Bcl-2 overexpression resulted in a retardation of the apoptotic process via prevention of cytochrome c release and caspases activation, and ceramide formation was also blocked when Bcl-2 was highly overexpressed in glioma cells. In addition, transient overexpression of Bcl-xL also exerted inhibitory effects on ceramide formation and apoptotic cell death induced by etoposide. These results indicate that Bax promotes apoptosis regardless of ceramide formation and that Bcl-2 or Bcl-xL prevents ceramide formation by repressing neutral sphingomyelinase as well as ceramide-induced cytochrome c release. Oncogene (2000) 19, 3508 - 3520 SN - 0950-9232 UR - https://www.unboundmedicine.com/medline/citation/10918609/Influence_of_Bax_or_Bcl_2_overexpression_on_the_ceramide_dependent_apoptotic_pathway_in_glioma_cells_ L2 - https://doi.org/10.1038/sj.onc.1203699 DB - PRIME DP - Unbound Medicine ER -