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人胃癌细胞系中FHIT转录本的异常剪接。

Aberrant splicing of FHIT transcripts in human gastric cancer cell lines.

作者信息

Lee Sang-Han, Kim Ho-Young, Kim Tae-Jung, Park Hyun-Kyoung, Kim Woo-Hyoung, Woo Kee-Min, Cho Man-Hee

机构信息

Department of Biochemistry, College of Medicine, Soonchunhyang University, Cheon-An 330-090, Korea.

出版信息

Res Commun Mol Pathol Pharmacol. 2002;112(1-4):39-49.

Abstract

Alterations of the FHIT gene occur as frequent events in several human cancers. Replacement of exogenous wild-type FHIT gene has been shown to induce suppression of tumorigenicity of human FHIT-negative cells in nude mice and aberrant FHIT transcripts have been observed in a variety of human solid tumors. In the presence study, we performed a nested reverse transcription-polymerase chain reaction (RT-PCR) analysis to identify aberrant FHIT transcripts in 6 gastric cancer cell lines. In addition to the wild-type FHIT transcript, small-sized transcripts with various number and lengths were observed in all of the cell lines examined. Sequence analysis confirmed that different types of truncated transcripts included exonic deletions, insertions of intron 5 sequences between exons, and combinations of both. Most of these transcripts lacked exon 5 in which translation initiation codon is located. Aberrant transcripts with partial exonic deletions, resulting from activation of cryptic splice sites, were also observed in 5 cell lines. Additionally, multi-step splice patterns, indicative of additional downstream processing, were observed in several cancer lines. Our results suggest that the aberrant FHIT transcripts in gastric cancer cell lines resulted from faulty splicing, including exon skipping, selection of cryptic splice site and additional downstream splice processing.

摘要

FHIT基因改变在几种人类癌症中频繁发生。研究表明,外源性野生型FHIT基因的替代可诱导人FHIT阴性细胞在裸鼠中的致瘤性受到抑制,并且在多种人类实体瘤中观察到异常的FHIT转录本。在本研究中,我们进行了巢式逆转录-聚合酶链反应(RT-PCR)分析,以鉴定6种胃癌细胞系中的异常FHIT转录本。除了野生型FHIT转录本外,在所有检测的细胞系中均观察到具有不同数量和长度的小尺寸转录本。序列分析证实,不同类型的截短转录本包括外显子缺失、外显子之间插入内含子5序列以及两者的组合。这些转录本中的大多数缺少包含翻译起始密码子的外显子5。在5个细胞系中还观察到由隐蔽剪接位点激活导致的具有部分外显子缺失的异常转录本。此外,在几个癌细胞系中观察到多步骤剪接模式,表明存在额外的下游加工。我们的结果表明,胃癌细胞系中的异常FHIT转录本是由错误剪接导致的,包括外显子跳跃、隐蔽剪接位点的选择和额外的下游剪接加工。

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