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Carcinogenesis Advance Access published online on March 24, 2005
Carcinogenesis, doi:10.1093/carcin/bgi075
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© The Author 2005. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oupjournals.org
Received January 3, 2005
Revised March 14, 2005
Accepted March 16, 2005

CANCER BIOLOGY

Deregulated expression of the PER1, PER2 and PER3 genes in breast cancers

Shou-Tung Chen 1, Kong-Bung Choo 2, Ming-Feng Hou 3, Kun-Tu Yeh 4, Shou-Jen Kuo 4, and Jan-Gowth Chang 5*

1 Department of Molecular Medicine, China Medical University Hospital, Taichung, Taiwan; Department of Surgery, Changhua Christian Hospital, Changhua, Taiwan; Department of Pathology, Changhua Christian Hospital, Changhua, Taiwan
2 Department of Medical Research and Education, Taipei Veterans General Hospital, Shih-Pai, Taipei, Taiwan
3 Department of Surgery, Kaohsiung Medical University, Kaohsiung, Taiwan
4 Department of Surgery, Changhua Christian Hospital, Changhua, Taiwan; Department of Pathology, Changhua Christian Hospital, Changhua, Taiwan
5 Department of Molecular Medicine, China Medical University Hospital, Taichung, Taiwan; Taipei Institute of Pathology, Taipei, Taiwan

* To whom correspondence should be addressed.
Jan-Gowth Chang, E-mail: d6781{at}www.cmuh.org.tw


  Abstract

Disruption of circadian rhythm may be a risk factor in the development of breast cancer, but molecular changes in circadian rhythm controlled genes in breast cancer cells are still unexplored. We used immunohistochemical staining, methylation specific PCR and direct sequencing methods to analyze molecular changes in three most important genes, namely PER1, PER2, and PER3, in circadian rhythm in 55 cases of breast cancer of Taiwanese women. Our results reveal disturbances in the expression of the three PER genes in most (over 95%) of breast cancerous cells in comparison with nearby non-cancerous cells. The PER gene deregulation is not caused by genetic mutations but most probably by methylation of the PER1 or PER2 promoter. Methylation of the PER gene promoters has a strong correlation with c-erbB2 expression (P=0.017). Because the circadian clock controls expression of cell cycle-related genes, we suggest that disturbances in PER gene expression may result in disruption of the control of the normal circadian clock hence benefiting the survival of cancer cells and promoting carcinogenesis. Differential expression of circadian genes in non-cancerous and cancerous cells may provide a molecular basis for chronotherapy of breast cancer.

Keywords: breast cancer; deregulation; PER genes; methylation; mutational analysis.
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