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Profiling of cell cycle genes of breast cells exposed to etodolac

  1. Author:
    Roy, D.
    Arason, G. A.
    Chowdhury, B.
    Mitra, A.
    Calaf, G. M.

  2. Author Address

    [Roy, D.] CUNY, Dept Nat Sci, Hostos Coll, Bronx, NY 10451 USA. [Roy, D.; Arason, G. A.] Manhattan Coll, Grad Biotechnol Program, Riverdale, NY USA. [Chowdhury, B.] NCI, Human Retrovirus Sect, Vaccine Branch, NIH, Frederick, MD 21701 USA. [Chowdhury, B.] Walter Reed Army Inst Res, Dept Cellular Injury, Silver Spring, MD USA. [Mitra, A.] Coll Mt St Vincent, Dept Chem, Riverdale, NY USA. [Calaf, G. M.] Columbia Univ, Ctr Radiol Res, Med Ctr, New York, NY 10032 USA. [Calaf, G. M.] Univ Tarapaca, Inst Alta Invest, Arica, Chile.;Roy, D, CUNY, Dept Nat Sci, Hostos Coll, Hostos Coll Campus,A-507E,475 Grand Concourse, Bronx, NY 10451 USA.;droy@hostos.cuny.edu
    1. Year: 2010
    2. Date: May
  2. Journal: Oncology Reports
    1. 23
    2. 5
    3. Pages: 1383-1391
  4. Type of Article: Article
  5. ISSN: 1021-335X
  1. Abstract:

    Breast cancer represents the second leading cause of cancer-related deaths in the world. There is increasing evidence that perturbation of cell cycle regulation is an important contributing factor to various cancer progression stages. There are key checkpoints in the cell cycle involving various regulatory proteins. The relationship between these cell cycle regulatory proteins and cell cycle arrest by cyclooxygenase (COX) inhibitors during neoplastic progression remains largely unknown. Preclinical studies and epidemiological investigations have consistently shown that nonsteroidal anti-inflammatory drugs have some anti-proliferative and anti-oxidative stress response on various tumors. In this study, the effect of etodolac, a 1,8-diethyl-1,3,4,9-tetrahydropyrano (3,4-beta) indole-1-acetic acid on signaling pathways was investigated by examining the differential expression of various cell cycle regulatory protein genes. A human cell cycle gene array was used to profile the expression of 96 genes involved in the cell cycle regulation. Differentially expressed genes were highly altered by etodolac treatment. Twenty-six genes were up- and 20 down-regulated with 0.5 and 2 mM etodolac treatment. respectively. Seven genes (ATM, BAX, CCNA2, CDC27, RAD50 and p21) were prominently altered, and six (ATM, CCND2, CCNF, CDC20, CDK1A and RAD50) were commonly altered with both concentrations. This finding indicated that etodolac could play a critical role on cancer cells by inducing cell death.

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  2. DOI: 10.3892/or_00000775
  3. View record in Web of Science®
  4. WOS: 000277075100027

Library Notes

  1. Fiscal Year: FY2009-2010
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