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Progesterone inhibition of MDM2 p90 protein in MCF-7 human breast cancer cell line is dependent on p53 levels | OMICS International | Abstract
ISSN: 1747-0862

Journal of Molecular and Genetic Medicine
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Short Article

Progesterone inhibition of MDM2 p90 protein in MCF-7 human breast cancer cell line is dependent on p53 levels

Moussa Alkhalaf 1*, Abdalla M El-Mowafy2 and Laila A Abou-Zeid3

1Department of Biochemistry, Faculty of Medicine, Mansoura University, Egypt

2Department of Applied Therapeutics, Faculty of Pharmacy, Kuwait University, P.O. Box 24923, Safat 13110, Kuwait.

3Department of Chemistry, Faculty of Pharmacy, Mansoura University, Egypt

*Corresponding Author:
Moussa Alkhalaf
Tel: +965 5319489
Fax: +965 5338908
Email: [email protected]

Received date: 11 April 2005; Revised date: 16 June 2005; Accepted daate: 20 June 2005, Available online 19 August 2005; Published date: 19 August 2005

© Copyright: Moussa Alkhalaf et al

Abstract

The mdm2 gene encodes several protein isoforms with different molecular weights (p90, p80, p76 and p57). MDM2 p90 (usually considered to be the major MDM2 protein) binds to and inactivates P53. We have recently shown that growth inhibition of MCF-7 human breast cancer cells by progesterone is associated with P53 down-regulation. In this work, we analyzed the expression pattern of MDM2 proteins in three human breast cancer cell lines by western blotting with anti-MDM2 antibodies. We found a prominent expression of MDM2 p57 protein in cell lines which have non-functional P53 protein (T47D and MDA-MB-231) as compared to the p90, p80 isoforms, whereas p90 was the major protein isoform in MCF-7 cells that contain functional P53 protein. When MCF-7 cells were treated with 100 nM of progesterone, MDM2 p90 was inhibited but the highly expressed MDM2 p57 isoform was not. The inhibition of MDM2 p90 protein by progesterone was abrogated in MCF-7 cells transfected with a P53 expressing vector. To our knowledge, this is the first report linking progesterone-induced growth inhibition with down-regulation of the MDM2 protein. We present evidence that reestablishing of P53 expression by transient transfection of P53 cDNA in these cells enhances the expression level of MDM2 p90 isoform. The data indicate that expression of MDM2 p90 is regulated through a P53-dependent pathway in response to progesterone

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