BCLAF1 and its splicing regulator SRSF10 regulate the tumorigenic potential of colon cancer cells
Xuexia Zhou,
Xuebing Li,
Yuanming Cheng,
Wenwu Wu,
Zhiqin Xie,
Qiulei Xi,
Jun Han,
Guohao Wu,
Jing Fang and
Ying Feng ()
Additional contact information
Xuexia Zhou: Key laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
Xuebing Li: Key laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
Yuanming Cheng: Key laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
Wenwu Wu: Key laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
Zhiqin Xie: Key laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
Qiulei Xi: Zhongshan Hospital, Fudan University School of Medicine
Jun Han: Zhongshan Hospital, Fudan University School of Medicine
Guohao Wu: Zhongshan Hospital, Fudan University School of Medicine
Jing Fang: Key laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
Ying Feng: Key laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
Nature Communications, 2014, vol. 5, issue 1, 1-11
Abstract:
Abstract Bcl-2-associated transcription factor 1 (BCLAF1) is known to be involved in multiple biological processes. Although several splice variants of BCLAF1 have been identified, little is known about how BCLAF1 splicing is regulated or the contribution of alternative splicing to its developmental functions. Here we find that inclusion of alternative exon5a was significantly increased in colorectal cancer (CRC) samples. Knockdown of the BCLAF1 protein isoform resulting from exon5a inclusion inhibited growth and that its overexpression increased tumorigenic potential. We also found that the splicing factor SRSF10 stimulates inclusion of exon5a and has growth-inducing activity. Importantly, the upregulation of SRSF10 expression observed in clinical CRC samples parallels the increased inclusion of BCLAF1 exon5a, both of which are associated with higher tumour grade. These findings identify SRSF10 as a key regulator of BCLAF1 pre-mRNA splicing and the maintenance of oncogenic features in human colon cancer cells.
Date: 2014
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms5581
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DOI: 10.1038/ncomms5581
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