Novel transcripts of fibroblast growth factor receptor 3 reveal aberrant splicing and activation of cryptic splice sequences in colorectal cancer.
Novel transcripts of fibroblast growth factor receptor 3 reveal aberrant splicing and activation of cryptic splice sequences in colorectal cancer.
复制标题
成纤维细胞生长因子受体 3 的新转录物揭示了结直肠癌中隐秘剪接序列的异常剪接和激活。
作者：
Jun;Ki;Young;Richard Lee;Wallace L. McKeehan;Jae
对人类结直肠癌FGFR3的巢式逆转录PCR分析揭示了由异常剪接和隐蔽剪接序列激活引起的新型突变转录本。两个异常剪接的转录本检测频率高，在50%的36个原发性肿瘤和60%的10人结直肠癌细胞系。大多数转录本使用正常的剪接位点，但跳过或包括外显子8和9。两个突变体转录本产生于外显子7中剪接到外显子10的隐蔽剪接供体位点。预测的翻译产物将在外显子10中表现出移码和提前终止密码子。我们认为mRNA剪接的失调经常产生异常的FGFR3转录物，这可能会在结直肠肿瘤发生中对细胞克隆产生可选择的优势。
A nested reverse transcription-PCR analysis of FGFR3 from human colorectal carcinomas revealed novel mutant transcripts caused by aberrant splicing and activation of cryptic splice sequences. Two aberrantly spliced transcripts were detected with high frequency in 50% of 36 primary tumors and in 60% of 10 human colorectal cancer cell lines. Most transcripts used normal splice sites but skipped or included exons 8 and 9. Two mutant transcripts arose from cryptic splice donor sites in exon 7 that spliced to exon 10. The predicted translation products would exhibit frameshifts and a premature termination codon in exon 10. We propose that dysregulation of mRNA splicing frequently generates an aberrant FGFR3 transcript that may confer a selectable advantage on clones of cells in colorectal tumorigenesis.
鉴定人结肠上皮中成纤维细胞生长因子受体 3 (FGFR3 IIIb) 的新型变异形式。
影响因子：
11.2
作者：
Murgue,B;Tsunekawa,S;Rosenberg,I;deBeaumont,M;Podolsky,DK
通讯作者：
Podolsky,DK
影响因子：
11.2
作者：
M. Kobrin;Y. Yamanaka;H. Friess;Martha E. Lopez;M. Korc
通讯作者：
M. Kobrin;Y. Yamanaka;H. Friess;Martha E. Lopez;M. Korc
DOI：
10.1152/ajpgi.1997.272.4.g885
发表时间：
1997-04-01
影响因子：
4.5
作者：
Kanai, M;Rosenberg, I;Podolsky, DK
通讯作者：
Podolsky, DK