Abstract
Alternative splicing and transcription elongation are vital biological process, which dysregulation causes multiple diseases including tumor. However, the co-regulation mechanism alternative splicing and transcription elongation in tumor remains unclear. This study demonstrates a novel alternative splicing pattern of ZO-1 regulated by RNAPII elongation rate in colorectal cancer (CRC). GLTSCR1 repressed the transcription elongation rate of ZO-1 to provide a time span for spliceosome recognizing the weak 3’and 5’splice sites of 23 rd exon, then splice factors HuR bound to the specific motif of ZO-1 22 nd intron to assist 23 rd exon inclusion. Since 23 rd exon inclusion of ZO-1 played a tumor suppression role in CRC, which might provide a novel potential therapeutic target for CRC. Funding: This work is supported by the National Natural Science Foundation of China (81871937, 82001586, 91859204, 82072629), CAMS Innovation Fund for Medical Sciences (CIFMS, 2019-I2M-5-044), the Natural Science Foundation of Zhejiang Province (LZ21H160001) and China Postdoctoral Science Foundation (2021M692797). Declaration of Interest: None to declare. Ethical Approval: This study was approved by the Ethics Committee of department of Medicine, Zhejiang University (2018-018)
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