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

23 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

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1002/ijc.20407

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

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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