Multifactorial mechanism for the potentiation of cisplatin (CDDP) cytotoxicity by all-trans retinoic acid (ATRA) in human ovarian carcinoma cell lines

Caliaro, M. J.; Vitaux, P.; Lafon, Corinne; Lochon, Isabelle; Nehmé, Alissar; Valette, Annie; Canal, Pierre; Bugat, R.; Jozan, S.

doi:10.1038/bjc.1997.55

Cited by 27 publications

(19 citation statements)

References 29 publications

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“…both retinoids differed in their potency to modulate CDDP sensitivity, indicating that additional mechanisms might be responsible for the potentiating effect of ATRA. This is supported by work from Caliaro et al (1997), who suggest that retinoid-mediated alteration of the glutathione-S-transferase activity accompanied by changes in platinum-DNA adduct formation and in epidermal growth factor receptor expression could account for the potentiation of CDDP cytotoxicity in ovarian cancer cells. Retinoids not only represent promising drugs for single-agent anti-cancer treatment.…”

Section: Discussionmentioning

confidence: 74%

Effects of retinoic acid and fenretinide on the c-erbB-2 expression, growth and cisplatin sensitivity of breast cancer cells

Grunt

Dittrich²,

Offterdinger³

et al. 1998

Br J Cancer

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Summary We investigated the effects of all-trans retinoic acid (ATRA) and fenretinide (4-HPR) on c-erbB-2 expression in SK-BR-3, and MCF-7 breast cancer cells and on the growth, differentiation, apoptosis and cisplatin (CDDP) sensitivity of SK-BR-3 cells. It has been reported that oestrogen inhibits c-erbB-2 in oestrogen receptor-positive breast cancer cells. Using ELISA, Westem and Northem analysis we have demonstrated that ATRA and 4-HPR exert similar effects down-regulating c-erbB-2 protein and mRNA in c-erbB-2-overexpressing SK-BR-3 and BT-474 and in normally expressing MCF-7 cells. Both retinoids inhibit SK-BR-3 cell growth. ATRA induces cellular enlargement and flattening, suggesting epithelial differentiation. 4-HPR causes nuclear and cytoplasmic condensation, DNA fragmentation and externalization of phosphabdylserine, indicating apoptosis. c-erbB-2 expression/activity has been linked to sensitivity against CDDP. Therefore, combinations of ATRA or 4-HPR with CDDP were tested for their anti-proliferative activity. Retinoid-conditioned cells were either exposed to retinoid and CDDP (schedule 1, 'continuous retinoid treatment') or to CDDP alone (schedule II, 'retinoid pretreatment'). This retinoid-conditioning followed by CDDP ± retinoid yields stronger growth inhibition compared with unconditioned cells, which were exposed to CDDP ± retinoid (schedule 111, 'no retnoid pretreatment'). The inefficacy of schedule Ill indicates that retioidconditioning is essential for the improvement of the antiproliferative effect. The interactions in schedules I and II are synergistic for ATRA and CDDP, but slightly antagonistic for 4-HPR and CDDP. However, 4-HPR + CDDP is more effective in growth inhibition than each drug alone.

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Section: Discussionmentioning

confidence: 74%

Effects of retinoic acid and fenretinide on the c-erbB-2 expression, growth and cisplatin sensitivity of breast cancer cells

Grunt

Dittrich²,

Offterdinger³

et al. 1998

Br J Cancer

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“…It is possible that DNA platination levels could be elevated as a consequence of hormone treatment, as suggested by reports that active promoter sites are preferentially platinated by the drug (42,43). We have investigated the bound-platinum levels on genomic DNA in cells treated with steroid hormones by platinum atomic absorption spectroscopy.…”

Section: Effects Of Hormones On Cell Proliferation and Sensitivity Tomentioning

confidence: 99%

Steroid hormones induce HMG1 overexpression and sensitize breast cancer cells to cisplatin and carboplatin

Liang²,

Lippard³

2000

Proc. Natl. Acad. Sci. U.S.A.

192

156

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Cisplatin is an anticancer drug that has enjoyed remarkable success against testicular tumors, but dose limiting side-effects have limited its application against a broader range of cancers. Previous studies have shown that high-mobility group (HMG) domain proteins such as HMG1 sensitize cells to cisplatin by shielding its major DNA adducts from nucleotide excision repair. Estrogen treatment increases HMG1 mRNA levels in breast cancer MCF-7 cells. Herein, we describe that treatment of human cancer cells having steroid hormone receptors with the appropriate hormone, estrogen and͞or progesterone, significantly increases the potency of cisplatin and its analogue carboplatin by causing the overexpression of HMG1. These findings suggest that the proper combination of these drugs, which are already approved by the Food and Drug Administration, could have potential benefit in treating tumors such as ovarian or breast that carry the hormone receptors.

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“…Recent studies have shown that ATRA enhances the cytotoxicity of chemotherapeutic agents. For instance, ATRA has been shown to increase the in vitro sensitivity to cisplatin in squamous head and neck cancer and in ovarian cancer cells (Sacks et al, 1995;Aebi et al, 1997;Caliaro et al, 1997). Formelli et al have demonstrated in an in vivo model that the synthetic retinoid fenretinide enhanced activity of cisplatin and increased survival of nude mice bearing ovarian carcinoma xenografts (Formelli and Cleris, 1993).…”

mentioning

confidence: 99%

Modulation of docetaxel-induced apoptosis and cell cycle arrest by all- trans retinoic acid in prostate cancer cells

et al. 2001

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We report that all- trans retinoic acid (ATRA) enhanced the toxicity of docetaxel against DU145 and LNCaP prostate cancer cells, and that the nature of the interaction between ATRA and docetaxel was highly synergistic. Docetaxel-induced apoptotic cell death was associated with phosphorylation and hence inactivation of Bcl-2. ATRA enhanced docetaxel-induced apoptosis and combined treatment with ATRA and docetaxel resulted in down-regulation of Bcl-2. Docetaxel caused phosphorylation and hence inactivation of cdc2 kinase result ing in G2/M arrest. ATRA inhibited docetaxel-induced phosphorylation of cdc2 resulting in activation of cdc2 kinase and partial reversal of the G2/M arrest. ATRA also inhibited docetaxel-induced activation of MAPK indicating that the effects of docetaxel and ATRA on cdc2 phosphorylation are dependent on MAPK. We conclude that ATRA synergistically enhances docetaxel toxicity by down-regulating Bcl-2 expression and partially reverses the docetaxel-induced G2/M arrest by inhibiting docetaxel-induced cdc2 phosphorylation in a pathway that is dependent on MAPK. ¬© 2001 Cancer Research Campaign http://www.bjcancer.com

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Multifactorial mechanism for the potentiation of cisplatin (CDDP) cytotoxicity by all-trans retinoic acid (ATRA) in human ovarian carcinoma cell lines

Cited by 27 publications

References 29 publications

Effects of retinoic acid and fenretinide on the c-erbB-2 expression, growth and cisplatin sensitivity of breast cancer cells

Effects of retinoic acid and fenretinide on the c-erbB-2 expression, growth and cisplatin sensitivity of breast cancer cells

Steroid hormones induce HMG1 overexpression and sensitize breast cancer cells to cisplatin and carboplatin

Modulation of docetaxel-induced apoptosis and cell cycle arrest by all- trans retinoic acid in prostate cancer cells

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