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Selenium effects on prostate cell growth.

D G Menter1, A L Sabichi, S M Lippman

  • 1Department of Clinical Cancer Prevention, The University of Texas M. D. Anderson Cancer Center, Houston 77030, USA.

Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology
|November 30, 2000
PubMed
Summary
This summary is machine-generated.

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Selenium compounds, sodium selenite (Na2SeO3) and l-selenomethionine (SeMet), selectively inhibit prostate cancer cell growth and induce apoptosis. SeMet shows particular promise for targeting cancer cells while sparing normal prostate cells.

Area of Science:

  • Oncology
  • Nutritional Biochemistry
  • Molecular Biology

Background:

  • Epidemiological studies suggest selenium's role in prostate cancer prevention.
  • The precise biological mechanisms of selenium's effects on prostate cells remain unclear.

Purpose of the Study:

  • To investigate the differential effects of sodium selenite (Na2SeO3) and l-selenomethionine (SeMet) on normal and cancerous prostate cell growth and survival.
  • To elucidate the molecular pathways involved in selenium-induced apoptosis in prostate cancer.

Main Methods:

  • Treatment of normal prostate primary cultures and prostate cancer cell lines (LNCaP, PC-3, DU145) with varying concentrations of Na2SeO3 and SeMet.
  • Assessment of cell viability, apoptosis (TUNEL assay, caspase-3 activation, PARP cleavage), cell cycle progression (flow cytometry), and anchorage-independent growth.

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  • Analysis of specific molecular markers like PARP expression and P-Tyr15-p34/cdc2 phosphorylation.

    • Main Results:

    • Both Na2SeO3 and SeMet demonstrated dose-dependent growth inhibition and apoptosis in prostate cancer cells, with Na2SeO3 being more potent overall.
    • Normal prostate cells exhibited significantly higher resistance to selenium-induced growth suppression compared to cancer cells.
    • SeMet selectively induced G2-M cell cycle arrest in cancer cells, linked to P-Tyr15-p34/cdc2 phosphorylation, and promoted apoptosis via PARP cleavage.
    • Anchorage-independent growth of prostate cancer cells was inhibited by selenium.

    Conclusions:

    • Sodium selenite and l-selenomethionine exhibit selective anti-cancer effects on prostate cells.
    • l-Selenomethionine demonstrates potential as a chemopreventive or therapeutic agent due to its selective induction of apoptosis and cell cycle arrest in cancer cells.
    • These findings provide insights into the molecular mechanisms underlying selenium's influence on prostate carcinogenesis.