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

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

doi:10.1002/ijc.20407

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

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

Research output: Contribution to journal › Article › peer-review

20 Citations (Scopus)

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 I 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 I was detected exclusively in lung cancer specimens (Il 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.

Original language	English
Pages (from-to)	8-13
Number of pages	6
Journal	International Journal of Cancer
Volume	112
Issue number	1
DOIs	https://doi.org/10.1002/ijc.20407
Publication status	Published - Oct 20 2004

Keywords

Alternative splicing
HELLS
Loss of heterozygosity
Lung cancer
SMARCA6

ASJC Scopus subject areas

Oncology
Cancer Research

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Tumor-specific exon creation of the HELLS/SMARCA6 gene in non-small cell lung cancer. / Yano, Masaaki; Ouchida, Mamoru; Shigematsu, Hisayuki; Tanaka, Noriyoshi; Ichimura, Koichi; Kobayashi, Kazuyasu; Inaki, Yasuhiko; Toyooka, Shinichi; Tsukuda, Kazunori; Shimizu, Nobuyoshi; Shimizu, Kenji.

In: International Journal of Cancer, Vol. 112, No. 1, 20.10.2004, p. 8-13.

Research output: Contribution to journal › Article › peer-review

Yano, Masaaki ; Ouchida, Mamoru ; Shigematsu, Hisayuki ; Tanaka, Noriyoshi ; Ichimura, Koichi ; Kobayashi, Kazuyasu ; Inaki, Yasuhiko ; Toyooka, Shinichi ; Tsukuda, Kazunori ; Shimizu, Nobuyoshi ; Shimizu, Kenji. / Tumor-specific exon creation of the HELLS/SMARCA6 gene in non-small cell lung cancer. In: International Journal of Cancer. 2004 ; Vol. 112, No. 1. pp. 8-13.

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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 I 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 I was detected exclusively in lung cancer specimens (Il 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.",

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