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BCLAF1 and its splicing regulator SRSF10 regulate the tumorigenic potential of colon cancer cells

Author

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  • 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
    Present address: Tianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenvironment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin 300052, China)

  • 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
    Key Laboratory of Food Safety Risk Assessment, Ministry of Health)

  • Ying Feng

    (Key laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
    Key Laboratory of Food Safety Risk Assessment, Ministry of Health)

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.

Suggested Citation

  • Xuexia Zhou & Xuebing Li & Yuanming Cheng & Wenwu Wu & Zhiqin Xie & Qiulei Xi & Jun Han & Guohao Wu & Jing Fang & Ying Feng, 2014. "BCLAF1 and its splicing regulator SRSF10 regulate the tumorigenic potential of colon cancer cells," Nature Communications, Nature, vol. 5(1), pages 1-11, December.
    • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms5581
    DOI: 10.1038/ncomms5581
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    Cited by:

    1. Cunjie Chang & Muthukumar Rajasekaran & Yiting Qiao & Heng Dong & Yu Wang & Hongping Xia & Amudha Deivasigamani & Minjie Wu & Karthik Sekar & Hengjun Gao & Mengqing Sun & Yuqin Niu & Qian Li & Lin Tao, 2022. "The aberrant upregulation of exon 10-inclusive SREK1 through SRSF10 acts as an oncogenic driver in human hepatocellular carcinoma," Nature Communications, Nature, vol. 13(1), pages 1-17, December.

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