Cell Death Mechanism Induced By 15-Deoxy Prostaglandin J2 And 17β-Estradiol In Er-Positive And Er-Negative Breast Cancer Cell Lines

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Date
2011-01
Authors
Aziz, Rabail Nasir
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Publisher
Universiti Sains Malaysia
Abstract
Breast cancer is the most common malignancy in Malaysian women. An increase in the prevalence of this disease worldwide indicates the necessity to explore and identify more potent and effective therapies against breast cancer. A number of studies are investigating drugs that cause no or minimal adverse effects and also focus on better understanding of the drug response and resistance by the tumour cells. Peroxisome proliferator-activated receptor gamma (PPARγ) is a ligand-dependent nuclear receptor which is reported to be expressed in various cancer cells including breast, prostate, colorectal and cervical cancer. Ligands for this receptor have been found to inhibit various cancer cell growth by inducing apoptosis and attenuating cellular proliferation following PPARγ activation. The exact role of this receptor and its ligands, however, remains to be elucidated, especially in breast cancer cells. The present study was carried out to explore the effect of an endogenous ligand of PPARγ, 15 deoxy-Prostaglandin J2 (15d-PGJ2) on the estrogen receptor (ER)-positive (MCF-7) and ER-negative (MDA-MB-231) human breast cancer cells in the presence and absence of an ERα ligand, 17β-estradiol (E2). The combined treatment of cells with 15d-PGJ2 and E2 was aimed to explore the recently reported existence of signalling cross-talk between PPARγ and ERα. Cytotoxicity analysis showed that 15d-PGJ2 inhibited MCF-7 and MDA-MB-231 cells proliferation at EC50 values of 15 and 10 μM, respectively.
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Keywords
15-Deoxy Prostaglandin J2 And 17β-Estradiol In Er-Positive , Breast Cancer Cell
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