Divergent biological effects of estradiol and diethylstilbestrol in the prostate cancer cell line MOP

Kalach, Jean-Jacques; Joly-Pharaboz, Marie-Odile; Chantepie, Jacqueline; Nicolas, Brigitte; Descôtes, Françoise; Mauduit, Claire; Benahmed, Mohamed; André, Jean

doi:10.1016/j.jsbmb.2005.02.012

Cited by 12 publications

(7 citation statements)

References 52 publications

(84 reference statements)

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“…In the presence of R1881 at 1 pM-10 nM, the growth curve LNCaP cells was characteristically bell-shaped, with a peak at 0.1 nM [30,31]. TRAIL, DR4 and DcR1 protein expressions were unaffected under these conditions, whereas DR5 and DcR2 protein expression increased over a nanomolar range.…”

Section: Discussionmentioning

confidence: 99%

Down-regulation of DcR2 sensitizes androgen-dependent prostate cancer LNCaP cells to TRAIL-induced apoptosis

et al. 2011

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BackgroundDysregulation of many apoptotic related genes and androgens are critical in the development, progression, and treatment of prostate cancer. The differential sensitivity of tumour cells to TRAIL-induced apoptosis can be mediated by the modulation of surface TRAIL receptor expression related to androgen concentration. Our previous results led to the hypothesis that downregulation of TRAIL-decoy receptor DcR2 expression following androgen deprivation would leave hormone sensitive normal prostate cells vulnerable to the cell death signal generated by TRAIL via its pro-apoptotic receptors. We tested this hypothesis under pathological conditions by exploring the regulation of TRAIL-induced apoptosis related to their death and decoy receptor expression, as also to hormonal concentrations in androgen-sensitive human prostate cancer, LNCaP, cells.ResultsIn contrast to androgen-insensitive PC3 cells, decoy (DcR2) and death (DR5) receptor protein expression was correlated with hormone concentrations and TRAIL-induced apoptosis in LNCaP cells. Silencing of androgen-sensitive DcR2 protein expression by siRNA led to a significant increase in TRAIL-mediated apoptosis related to androgen concentration in LNCaP cells.ConclusionsThe data support the hypothesis that hormone modulation of DcR2 expression regulates TRAIL-induced apoptosis in LNCaP cells, giving insight into cell death induction in apoptosis-resistant hormone-sensitive tumour cells from prostate cancer. TRAIL action and DcR2 expression modulation are potentially of clinical value in advanced tumour treatment.

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Section: Discussionmentioning

confidence: 99%

Down-regulation of DcR2 sensitizes androgen-dependent prostate cancer LNCaP cells to TRAIL-induced apoptosis

et al. 2011

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“…The variants 104-R [3,8], LNCaP-abl 75 cells [6] and MOP cells [9] emerged after culturing for several months in androgen-poor culture medium. The effects of estradiol were similar to those of androgens possibly because these cells carried the T877A-mutated AR [4,[9][10][11]. The ARCaP cells [5], also known as MDA Pca1 [12], were derived from the ascites fluid of a patient with metastases to the liver, spine and long bones.…”

Section: Introductionmentioning

confidence: 98%

Androgen inhibits the growth of carcinoma cell lines established from prostate cancer xenografts that escape androgen treatment

Joly-Pharaboz

Kalach

Pharaboz

et al. 2008

The Journal of Steroid Biochemistry and Molecular Biology

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“…The diarylethylene moiety in both combretastatin A-4 (CA4)2 and diethylstilbestrol (DES)3 (Fig. 1) inspired us to modify the molecular templates found in certain non-steroidal antiestrogenic compounds to explore the interaction of the resulting new compounds with the tubulin-microtubule protein system.…”

Section: Introductionmentioning

confidence: 99%

Application of the McMurry coupling reaction in the synthesis of tri- and tetra-arylethylene analogues as potential cancer chemotherapeutic agents

Tanpure¹,

Harkrider²,

Strecker³

et al. 2009

Bioorganic & Medicinal Chemistry

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Structural redesign of selected non-steroidal estrogen receptor binding compounds has previously been successful in the discovery of new inhibitors of tubulin assembly. Accordingly, tetra-substituted alkene analogues (21-30) were designed based in part on combinations of the structural and electronic components of tamoxifen and combretastatin A-4 (CA4). The McMurry coupling reaction was used as the key synthetic step in the preparation of these tri-and tetra-arylethylene analogues. The structural assignment of E, Z isomers was determined on the basis of 2D-NOESY experiments. The ability of these compounds to inhibit tubulin polymerization and cell growth in selected human cancer cell lines was evaluated. Although the compounds were found to be less potent than CA4, these analogues significantly advance the known structure activity relationship associated with the colchicine binding site on β-tubulin.

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Divergent biological effects of estradiol and diethylstilbestrol in the prostate cancer cell line MOP

Cited by 12 publications

References 52 publications

Down-regulation of DcR2 sensitizes androgen-dependent prostate cancer LNCaP cells to TRAIL-induced apoptosis

Down-regulation of DcR2 sensitizes androgen-dependent prostate cancer LNCaP cells to TRAIL-induced apoptosis

Androgen inhibits the growth of carcinoma cell lines established from prostate cancer xenografts that escape androgen treatment

Application of the McMurry coupling reaction in the synthesis of tri- and tetra-arylethylene analogues as potential cancer chemotherapeutic agents

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