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Infrequent hypermethylation of the PTEN gene in Korean non‐small‐cell lung cancers
Author(s) -
Kim Dong Sun,
Lee Su Man,
Yoon Ghil Suk,
Choi Jin Eun,
Park Jae Yong
Publication year - 2010
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/j.1349-7006.2009.01406.x
Subject(s) - pten , medicine , cancer research , lung cancer , lung , oncology , pathology , biology , genetics , pi3k/akt/mtor pathway , apoptosis
CpG islands (CGIs) hypermethylation is implicated in the pathogenesis of many cancers, including lung cancer. The phosphate and tension homolog (PTEN) is a tumor suppressor that controls a variety of biological processes including cell proliferation, growth, migration, and death. The defects in PTEN regulation have a profound impact on carcinogenesis. Herein, we have examined the methylation status of the human PTEN gene in 137 primary non‐small‐cell lung cancers (NSCLCs) by using a methylation‐specific PCR and correlated the results with clinicopathological features. Promoter methylation of the PTEN gene was observed in 5.1%, 2.9%, and 0.0% of three different CpG regions, which were localized at −1460 to −1263, −984 to −848, and −300 to −128 nucleotides upstream of the translation start site, respectively. Reverse transcription‐PCR and immunohistochemical analysis showed the methylation of the CGI region at −984 to −848 correlated more accurately with PTEN expression. In addition, no significant correlation was found between PTEN methylation and clinicopathological factors, including the survival rates. These findings suggest that promoter methylation is not an important mechanism for PTEN deregulation in NSCLCs from Koreans. ( Cancer Sci 2010; 101: 568–572)

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