Cell cycle arrest biomarkers in human lung cancer cells after treatment with selenium in culture.

Abstract

In the planning of future intervention trials using chemopreventive agents against lung cancer, it is critical to evaluate the effect on biomarkers implicated specifically in lung carcinogenesis. With the use of the H520 and H522 human lung cancer cell lines, the present study showed that treatment with selenium (in the form of methylseleninic acid) inhibited cell growth, arrested cell cycle progression at G(1), and induced apoptosis as a late event. Because H520 cells were more sensitive to selenium than H522 cells (IC(50) of MSA was 2.5 or 10 micro M for H520 or H522 cells, respectively, at 24 h), a panel of nine cell cycle regulatory proteins known to be involved in G(1)-->S transition was assessed by Western analysis using whole cell lysate from H520 cells. These nine proteins (DP1, cdc25A, cyclin A, cyclin B(1), cyclin D(1), cdk1, cdk5, p21(WAF1), and GADD153) have been reported previously by our laboratory to be modulated by MSA in human breast and prostate cancer cells. Our data showed that only four (DP1, cdc25A, p21(WAF1), and GADD153) of nine biomarkers produced the expected changes after treatment of lung cancer cells with MSA. This finding raises the possibility that the molecular targets sensitive to selenium modulation may be tissue specific. Thus, the selection of selenium biomarkers for evaluation in an intervention trial must be based on empirical data derived from the cancer cell type of interest.

• Authors: Helen Swede, Yan Dong, Mary Reid, James Marshall, Clement Ip
• Journal: Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology (Cancer Epidemiol Biomarkers Prev) Vol. 12 Issue 11 Pt 1 Pg. 1248-52 (Nov 2003) ISSN: 1055-9965 [Print] United States
• PMID: 14652289 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Biomarkers
• Selenium

Topics

• Adenocarcinoma (genetics, pathology)
• Biomarkers (analysis)
• Blotting, Western
• Carcinoma, Non-Small-Cell Lung (genetics, pathology)
• Carcinoma, Squamous Cell (genetics, pathology)
• Cell Cycle (genetics, physiology)
• Cell Transformation, Neoplastic
• Chemoprevention
• Clinical Trials as Topic
• Endpoint Determination
• Humans
• Lung Neoplasms (genetics, pathology)
• Selenium (pharmacology)
• Tumor Cells, Cultured