Androgens Induce Resistance to bcl-2-mediated Apoptosis in LNCaP Prostate Cancer Cells

Guy J. Berchem; Manon Bosseler; La Vencia Y. Sugars; H. James Voeller; Samantha Zeitlin; Edward P. Gelmann

Androgens Induce Resistance to bcl-2-mediated Apoptosis in LNCaP Prostate Cancer Cells

Guy J. Berchem, Manon Bosseler, La Vencia Y. Sugars, H. James Voeller, Samantha Zeitlin, Edward P. Gelmann

Research output: Contribution to journal › Article › peer-review

Abstract

We describe an in vitro model for prostate cancer treatment that suggests a potential benefit for combined androgen ablation and cytotoxic chemotherapy. Androgen treatment of the LNCaP hormone-dependent human prostate cancer cell line induces increased expression of the BCL-2 protein. Increased levels of this protein are known to mediate inhibition of apoptosis. LNCaP cells, however, did not undergo apoptosis in response to androgen withdrawal. Etoposide exerts its cytotoxicity on LNCaP and other cells by inducing apoptosis. In vitro etoposide cytotoxicity was diminished 83% in the presence of either 10^-8 M dihydrotestosterone or 10^-9 M R1881 in LNCaP cells. The interaction between androgen and etoposide was mediated through the BCL-2 protein, since bcl-2 antisense oligonucleotides blocked the protective effect of androgens on etoposide cytotoxicity.

Original language	English (US)
Pages (from-to)	735-738
Number of pages	4
Journal	Cancer Research
Volume	55
Issue number	4
State	Published - Feb 15 1995
Externally published	Yes

ASJC Scopus subject areas

Oncology
Cancer Research

Cite this

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title = "Androgens Induce Resistance to bcl-2-mediated Apoptosis in LNCaP Prostate Cancer Cells",

abstract = "We describe an in vitro model for prostate cancer treatment that suggests a potential benefit for combined androgen ablation and cytotoxic chemotherapy. Androgen treatment of the LNCaP hormone-dependent human prostate cancer cell line induces increased expression of the BCL-2 protein. Increased levels of this protein are known to mediate inhibition of apoptosis. LNCaP cells, however, did not undergo apoptosis in response to androgen withdrawal. Etoposide exerts its cytotoxicity on LNCaP and other cells by inducing apoptosis. In vitro etoposide cytotoxicity was diminished 83% in the presence of either 10-8 M dihydrotestosterone or 10-9 M R1881 in LNCaP cells. The interaction between androgen and etoposide was mediated through the BCL-2 protein, since bcl-2 antisense oligonucleotides blocked the protective effect of androgens on etoposide cytotoxicity.",

author = "Berchem, {Guy J.} and Manon Bosseler and Sugars, {La Vencia Y.} and Voeller, {H. James} and Samantha Zeitlin and Gelmann, {Edward P.}",

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T1 - Androgens Induce Resistance to bcl-2-mediated Apoptosis in LNCaP Prostate Cancer Cells

AU - Berchem, Guy J.

AU - Bosseler, Manon

AU - Sugars, La Vencia Y.

AU - Voeller, H. James

AU - Zeitlin, Samantha

AU - Gelmann, Edward P.

PY - 1995/2/15

Y1 - 1995/2/15

N2 - We describe an in vitro model for prostate cancer treatment that suggests a potential benefit for combined androgen ablation and cytotoxic chemotherapy. Androgen treatment of the LNCaP hormone-dependent human prostate cancer cell line induces increased expression of the BCL-2 protein. Increased levels of this protein are known to mediate inhibition of apoptosis. LNCaP cells, however, did not undergo apoptosis in response to androgen withdrawal. Etoposide exerts its cytotoxicity on LNCaP and other cells by inducing apoptosis. In vitro etoposide cytotoxicity was diminished 83% in the presence of either 10-8 M dihydrotestosterone or 10-9 M R1881 in LNCaP cells. The interaction between androgen and etoposide was mediated through the BCL-2 protein, since bcl-2 antisense oligonucleotides blocked the protective effect of androgens on etoposide cytotoxicity.

AB - We describe an in vitro model for prostate cancer treatment that suggests a potential benefit for combined androgen ablation and cytotoxic chemotherapy. Androgen treatment of the LNCaP hormone-dependent human prostate cancer cell line induces increased expression of the BCL-2 protein. Increased levels of this protein are known to mediate inhibition of apoptosis. LNCaP cells, however, did not undergo apoptosis in response to androgen withdrawal. Etoposide exerts its cytotoxicity on LNCaP and other cells by inducing apoptosis. In vitro etoposide cytotoxicity was diminished 83% in the presence of either 10-8 M dihydrotestosterone or 10-9 M R1881 in LNCaP cells. The interaction between androgen and etoposide was mediated through the BCL-2 protein, since bcl-2 antisense oligonucleotides blocked the protective effect of androgens on etoposide cytotoxicity.

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Androgens Induce Resistance to bcl-2-mediated Apoptosis in LNCaP Prostate Cancer Cells

Abstract

ASJC Scopus subject areas

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