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Epigenetic silencing of the PRSS3 putative tumor suppressor gene in non‐small cell lung cancer
Author(s) -
Marsit Carmen J.,
Okpukpara Chinedu,
Danaee Hadi,
Kelsey Karl T.
Publication year - 2005
Publication title -
molecular carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.254
H-Index - 97
eISSN - 1098-2744
pISSN - 0899-1987
DOI - 10.1002/mc.20125
Subject(s) - biology , dna methylation , lung cancer , epigenetics , gene silencing , cancer research , fhit , methylation , tumor suppressor gene , cancer , adenocarcinoma , biomarker , gene , gene expression , carcinogenesis , genetics , oncology , medicine
The serine protease family member PRSS3 ( trypsinogen‐IV ) has been implicated as a putative tumor suppressor gene due to its loss of expression, which is correlated with promoter hypermethylation, in esophageal squamous cell carcinoma and gastric adenocarcinoma. As epigenetic alteration is common in non‐small cell lung cancer (NSCLC), we sought to determine if promoter hypermethylation of PRSS3 occurred in this disease, and if it was associated with clinical features of NSCLC or tobacco‐related exposures in these patients. Using methylation‐specific PCR, we determined the promoter hypermethylation status of PRSS3 in a case series study of primary NSCLC, and found methylation of this gene to be common, occurring in 53% (86 of 166) of tumors examined. There was no association of this alteration with patient demographics, tumor features, or exposure histories of the patients. The lack of association is of interest, as it may suggest a lack of specific selection for inactivation of this gene. On the other hand, the high prevalence of this alteration makes PRSS3 methylation an attractive biomarker for use in diagnostic or screening applications in NSCLC. © 2005 Wiley‐Liss, Inc.