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Tumor-specific exon creation of the HELLS/SMARCA6 gene in non-small cell lung cancer

✍ Scribed by Masaaki Yano; Mamoru Ouchida; Hisayuki Shigematsu; Noriyoshi Tanaka; Koichi Ichimura; Kazuyasu Kobayashi; Yasuhiko Inaki; Shinichi Toyooka; Kazunori Tsukuda; Nobuyoshi Shimizu; Kenji Shimizu

Publisher
John Wiley and Sons
Year
2004
Tongue
French
Weight
384 KB
Volume
112
Category
Article
ISSN
0020-7136

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✦ Synopsis

Abstract

To identify tumor‐suppressor genes on chromosome 10 in non‐small cell lung cancers, we isolated 10 types of splicing variant of the HELLS/SMARCA6 gene transcripts. HELLS/SMARCA6 is a novel member of SNF2 family, which is implicated in cellular functions like chromatin remodeling. Variant 1 was an alternatively spliced isoform containing an insertion of a 44 ntd intronic sequence between exons 3 and 4, giving rise to a premature termination of translation. Expression of variant 1 was detected exclusively in lung cancer specimens (11 of 43 cases, 26%) but was not detected in corresponding normal tissues. The D10S520 marker in the proximity of the HELLS/SMARCA6 gene showed prevalent allelic loss (41%) compared to flanking markers (25–31%). These results suggest that loss of function of HELLS/SMARCA6 by allelic loss and aberrant proteins by tumor‐specific exon creation may result in epigenetic deregulation, leading lung cells to malignancy or its progression. © 2004 Wiley‐Liss, Inc.

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