Format

Send to

Choose Destination
See comment in PubMed Commons below
J Cancer Res Clin Oncol. 2013 Mar;139(3):485-90. doi: 10.1007/s00432-012-1353-5. Epub 2012 Nov 22.

Frequent epigenetic silencing of PCDH10 by methylation in human colorectal cancer.

Author information

1
Cancer Institute (Key Laboratory for Cancer Intervention and Prevention, China National Ministry of Education), Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang Province, China.

Abstract

PURPOSE:

Aberrant DNA methylation is common in cancer cells. Epigenetic alterations resulting in the loss of tumor suppression gene functions are frequently involved in tumor development and progression. Recently, methylation of PCDH10 was reported to be associated with multiple hematologic malignancies as well as some solid tumors. Whether the down-regulation of PCDH10 happens in CRC remains unknown.

METHODS:

Methylation status of PCDH10 was evaluated by methylation-specific PCR analysis. The effects of PCDH10 re-expression were determined in growth, colony formation, cell cycle, and invasion assays.

RESULTS:

In this study, we found that 100 % (8 of 8) of colorectal cancer cell lines were silenced for PCDH10, but not normal colorectal epithelial cells. Demethylation treatment confirmed that the reduced expression is associated closely with promoter methylation. Hyper-methylation of PCDH10 was also detected in 85 % of primary colorectal tumors, but not in adjacent normal colorectal tissues.

CONCLUSIONS:

Our results suggest that PCDH10 is an important tumor suppression gene with key roles of suppressing cell proliferation, clonogenicity, and inhibiting cell invasion in the development of colorectal cancer. Thus, PCDH10 methylation may constitute a useful biomarker of colorectal cancer patients.

PMID:
23180019
DOI:
10.1007/s00432-012-1353-5
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Springer
    Loading ...
    Support Center