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Hypericin-induced apoptosis of human malignant glioma cells is light-dependent, independent of bcl-2 expression, and does not require wild-type p53

Standard

Hypericin-induced apoptosis of human malignant glioma cells is light-dependent, independent of bcl-2 expression, and does not require wild-type p53. / Weller, M; Trepel, M; Grimmel, C; Schabet, M; Bremen, D; Krajewski, Stan; Reed, John C.

in: NEUROL RES, Jahrgang 19, Nr. 5, 10.1997, S. 459-70.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Weller, M, Trepel, M, Grimmel, C, Schabet, M, Bremen, D, Krajewski, S & Reed, JC 1997, 'Hypericin-induced apoptosis of human malignant glioma cells is light-dependent, independent of bcl-2 expression, and does not require wild-type p53', NEUROL RES, Jg. 19, Nr. 5, S. 459-70.

APA

Weller, M., Trepel, M., Grimmel, C., Schabet, M., Bremen, D., Krajewski, S., & Reed, J. C. (1997). Hypericin-induced apoptosis of human malignant glioma cells is light-dependent, independent of bcl-2 expression, and does not require wild-type p53. NEUROL RES, 19(5), 459-70.

Vancouver

Weller M, Trepel M, Grimmel C, Schabet M, Bremen D, Krajewski S et al. Hypericin-induced apoptosis of human malignant glioma cells is light-dependent, independent of bcl-2 expression, and does not require wild-type p53. NEUROL RES. 1997 Okt;19(5):459-70.

Bibtex

@article{68de185b0135463faed41aad70589b1f,
title = "Hypericin-induced apoptosis of human malignant glioma cells is light-dependent, independent of bcl-2 expression, and does not require wild-type p53",
abstract = "Hypericin and tamoxifen are experimental agents for the adjuvant chemotherapy of malignant glioma. We report that hypericin and tamoxifen induce apoptosis of 7 human malignant glioma cell lines in a concentration- and time-dependent manner. Illumination is essential for the cytotoxicity of hypericin but not tamoxifen. Apoptosis is unaffected by inhibitors of RNA and protein synthesis or free radical scavengers, does not require wild-type p53 activity, and occurs in glioma cells expressing high levels of bcl-2. There is no correlation between hypericin and tamoxifen-induced cytotoxicity and inhibition of protein kinase C (PKC). Ectopic expression of a murine bcl-2 transgene provides modest protection from tamoxifen but does not affect hypericin toxicity. Hypericin and tamoxifen do not modulate glioma cell killing induced by tumor necrosis factor-alpha (TNF-alpha) or CD95 ligand. Both drugs augment the acute cytotoxicity of various cancer chemotherapy drugs but fail to shift their EC50 values in modified colony formation assays. These data do not provide further supportive evidence how to enhance the limited efficacy of tamoxifen treatment for human malignant glioma. However, hypericin is a promising agent for the treatment of malignant glioma if local photodynamic activation of hypericin in the glioma tissue can be achieved.",
keywords = "Antibiotics, Antineoplastic, Antigens, CD95, Antineoplastic Agents, Antineoplastic Agents, Hormonal, Apoptosis, Cell Division, Drug Resistance, Glioma, Humans, Light, Naphthalenes, Perylene, Protein Kinase C, Protein Synthesis Inhibitors, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-bcl-2, RNA, Tamoxifen, Tumor Cells, Cultured, Tumor Suppressor Protein p53, bcl-2-Associated X Protein, Journal Article, Research Support, Non-U.S. Gov't",
author = "M Weller and M Trepel and C Grimmel and M Schabet and D Bremen and Stan Krajewski and Reed, {John C}",
year = "1997",
month = oct,
language = "English",
volume = "19",
pages = "459--70",
number = "5",

}

RIS

TY - JOUR

T1 - Hypericin-induced apoptosis of human malignant glioma cells is light-dependent, independent of bcl-2 expression, and does not require wild-type p53

AU - Weller, M

AU - Trepel, M

AU - Grimmel, C

AU - Schabet, M

AU - Bremen, D

AU - Krajewski, Stan

AU - Reed, John C

PY - 1997/10

Y1 - 1997/10

N2 - Hypericin and tamoxifen are experimental agents for the adjuvant chemotherapy of malignant glioma. We report that hypericin and tamoxifen induce apoptosis of 7 human malignant glioma cell lines in a concentration- and time-dependent manner. Illumination is essential for the cytotoxicity of hypericin but not tamoxifen. Apoptosis is unaffected by inhibitors of RNA and protein synthesis or free radical scavengers, does not require wild-type p53 activity, and occurs in glioma cells expressing high levels of bcl-2. There is no correlation between hypericin and tamoxifen-induced cytotoxicity and inhibition of protein kinase C (PKC). Ectopic expression of a murine bcl-2 transgene provides modest protection from tamoxifen but does not affect hypericin toxicity. Hypericin and tamoxifen do not modulate glioma cell killing induced by tumor necrosis factor-alpha (TNF-alpha) or CD95 ligand. Both drugs augment the acute cytotoxicity of various cancer chemotherapy drugs but fail to shift their EC50 values in modified colony formation assays. These data do not provide further supportive evidence how to enhance the limited efficacy of tamoxifen treatment for human malignant glioma. However, hypericin is a promising agent for the treatment of malignant glioma if local photodynamic activation of hypericin in the glioma tissue can be achieved.

AB - Hypericin and tamoxifen are experimental agents for the adjuvant chemotherapy of malignant glioma. We report that hypericin and tamoxifen induce apoptosis of 7 human malignant glioma cell lines in a concentration- and time-dependent manner. Illumination is essential for the cytotoxicity of hypericin but not tamoxifen. Apoptosis is unaffected by inhibitors of RNA and protein synthesis or free radical scavengers, does not require wild-type p53 activity, and occurs in glioma cells expressing high levels of bcl-2. There is no correlation between hypericin and tamoxifen-induced cytotoxicity and inhibition of protein kinase C (PKC). Ectopic expression of a murine bcl-2 transgene provides modest protection from tamoxifen but does not affect hypericin toxicity. Hypericin and tamoxifen do not modulate glioma cell killing induced by tumor necrosis factor-alpha (TNF-alpha) or CD95 ligand. Both drugs augment the acute cytotoxicity of various cancer chemotherapy drugs but fail to shift their EC50 values in modified colony formation assays. These data do not provide further supportive evidence how to enhance the limited efficacy of tamoxifen treatment for human malignant glioma. However, hypericin is a promising agent for the treatment of malignant glioma if local photodynamic activation of hypericin in the glioma tissue can be achieved.

KW - Antibiotics, Antineoplastic

KW - Antigens, CD95

KW - Antineoplastic Agents

KW - Antineoplastic Agents, Hormonal

KW - Apoptosis

KW - Cell Division

KW - Drug Resistance

KW - Glioma

KW - Humans

KW - Light

KW - Naphthalenes

KW - Perylene

KW - Protein Kinase C

KW - Protein Synthesis Inhibitors

KW - Proto-Oncogene Proteins

KW - Proto-Oncogene Proteins c-bcl-2

KW - RNA

KW - Tamoxifen

KW - Tumor Cells, Cultured

KW - Tumor Suppressor Protein p53

KW - bcl-2-Associated X Protein

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

M3 - SCORING: Journal article

C2 - 9329022

VL - 19

SP - 459

EP - 470

IS - 5

ER -