Tyrphostins and retinoids cooperate during inhibition of in vitro growth of ovarian cancer cells

Chemoresistance of ovarian cancer can be overcome by co-administration of retinoids, albeit clinical proof of this hypothesis is pending. Moreover, growth factor/c-erbB signaling is crucial for ovarian tumor growth/chemosensitivity. Retinoids and c-erbB modulators therefore represent promising drugs...

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Bibliographic Details
Published in:Cancer letters 2003-01, Vol.189 (2), p.147-156
Main Author: Grunt, Thomas W
Format: Article
Language:English
Subjects:
Adenocarcinoma - enzymology
Adenocarcinoma - pathology
Antineoplastic agents
Apoptosis - drug effects
Benzothiazoles
Biological and medical sciences
C-erbB
Cell Division - drug effects
Cell growth
Chemotherapy
Drug Resistance, Neoplasm
Drug Synergism
ErbB Receptors - antagonists & inhibitors
Female
Humans
Kinases
Medical sciences
Neoplasm Proteins - antagonists & inhibitors
Ovarian cancer
Ovarian Neoplasms - enzymology
Ovarian Neoplasms - pathology
Pharmacology. Drug treatments
Quinazolines - pharmacology
Receptor, ErbB-2 - antagonists & inhibitors
Retinoic acid receptors
Retinoid
Rodents
Tretinoin - pharmacology
Tumor Cells, Cultured - cytology
Tumor Cells, Cultured - drug effects
Tumor Cells, Cultured - enzymology
Tyrphostin
Tyrphostins - pharmacology
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Summary:Chemoresistance of ovarian cancer can be overcome by co-administration of retinoids, albeit clinical proof of this hypothesis is pending. Moreover, growth factor/c-erbB signaling is crucial for ovarian tumor growth/chemosensitivity. Retinoids and c-erbB modulators therefore represent promising drugs for ovarian cancer. We demonstrate that c-erbB-1 (RG-14620, AG1517) and c-erbB-2 selective tyrphostins (AG825, AG879), and all- trans and 9- cis retinoic acid inhibit ovarian cancer cell proliferation (HOC-7, OVCAR-3). Unlike retinoids, AG1517 and AG879 induce apoptosis. The antiproliferative activity of AG1517 is enhanced by all- trans retinoic acid suggesting that c-erbB and retinoid pathways interact. Thus, these agents cooperate during ovarian cancer cell growth inhibition.
ISSN:0304-3835
1872-7980
DOI:10.1016/S0304-3835(02)00512-8