Overexpression of Cyclin E and its Low Molecular Weight Isoforms Cooperate with Loss of p53 in Promoting Oncogenic Properties of MCF-7 Breast Cancer Cells

Montazeri, Hamed; Bouzari, Saeid; Azadmanesh, Kayhan; Ostad, Seyed Nasser; Ghahremani, Mohammad Hossein

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저자정보: Montazeri, Hamed (Department of Molecular Biology, Pasteur Institute of Iran) Bouzari, Saeid (Department of Molecular Biology, Pasteur Institute of Iran) Azadmanesh, Kayhan (Department of Virology, Pasteur Institute of Iran) Ostad, Seyed Nasser (Department of Toxicology-Pharmacology, Pharmacy, Tehran University of Medical Sciences) Ghahremani, Mohammad Hossein (Department of Toxicology-Pharmacology, Pharmacy, Tehran University of Medical Sciences)

저널정보: 아시아태평양암예방학회 Asian Pacific journal of cancer prevention : APJCP Asian Pacific journal of cancer prevention : APJCP 제16권 제17호

발행연도: 2015.1

수록면: 7,575 - 7,582 (8page)

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Cyclin E, a key coordinator of the G1 to S transition in the cell cycle, may be deregulated in several malignancies, including breast cancer. The most significant aberration in cyclin E is its elastase mediated proteolytic cleavage into tumor specific low molecular weight isoforms (LMW-Es). LMW-Es are biochemically hyperactive and biologically drive tumorigenesis in transgenic mouse models. Additionally, expression of LMW-Es has been correlated with poor survival in breast cancer cases. Here we determine whether expression of LMW-Es in a breast cancer cell line that is naturally devoid of these deregulated forms would alter their progression through each phase of the cell cycle. The results revealed that LMW-Es expression resulted in an increased doubling time, concomitant with a predominant increase in the population in the S phase of the cell cycle. Moreover, downregulation of p53 in LMW-Es cells resulted in additional shortening of the doubling time and enrichment of cells in the S and G2/M phases of the cell cycle. Furthermore, expression of LMW-Es sensitized cells to ${\beta}$-estradiol (E2) mediated growth and changed expression patterns of estrogen receptor and Bcl-2. Intriguingly, expression of LMW-Es could surpass anti-apoptotic effects raised by p53 upregulation. Taken together these studies suggest that overexpression of LMW-Es in collaboration with p53 loss results in altered g rowth properties of MCF-7 cells, enhancing the oncogenic activity of these ER positive breast cancer cells.

#Cyclin E #breast cancer #low molecular weight isoforms #p53 #estrogen receptor

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