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Genetic and epigenetic inactivation of LTF gene at 3p21.3 in lung cancers
Author(s) -
Iijima Hironobu,
Tomizawa Yoshio,
Iwasaki Yasuki,
Sato Koji,
Sunaga Noriaki,
Dobashi Kunio,
Saito Ryusei,
Nakajima Takashi,
Minna John D.,
Mori Masatomo
Publication year - 2005
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.21462
Subject(s) - trichostatin a , lung cancer , cancer research , biology , epigenetics , frameshift mutation , loss of heterozygosity , gene , microbiology and biotechnology , mutation , genetics , allele , pathology , medicine , histone deacetylase , histone
Allelic loss on the short arm of chromosome 3 is one of the most common events in the pathogenesis of lung cancer. The lactotransferrin gene ( LTF, also referred to as the lactoferrin gene, LF ) is located at 3p21.3 common eliminated region 1, which is frequently deleted in lung and other cancers. The expression of the LTF gene was absent in 16 (59%) of 27 small cell lung cancer cell lines, 33 (77%) of 43 nonsmall‐cell lung cancer (NSCLC) cell lines and 7 (54%) of 13 primary NSCLC, while LTF mRNA was overexpressed in 3 (7%) of 43 NSCLC cell lines. Its expression was restored by treatment with 5‐aza‐2′‐deoxycytidine (5‐aza‐dC), trichostatin A (TSA) or a combination of both in a subset of lung cancer cell lines without LTF expression. In addition, we found 8 different types of nucleotide substitutions and one frameshift mutation. These results indicate that the LTF gene is inactivated by genetic and epigenetic mechanisms in lung cancer. © 2005 Wiley‐Liss, Inc.