GLTSCR1 coordinates alternative splicing and transcription elongation of ZO1 to regulate colorectal cancer progression
作者机构：Department of Pathology and Women’s HospitalZhejiang University School of MedicineResearch Unit of Intelligence Classification of Tumor Pathology and Precision TherapyChinese Academy of Medical Sciences(2019RU042)Hangzhou 310058China Cancer Epigenetics ProgramWuxi School of MedicineJiangnan UniversityWuxi 214122China Key Laboratory of Disease Proteomics of Zhejiang ProvinceZhejiang UniversityHangzhou 310058China Cancer CenterZhejiang UniversityHangzhou 310058China Department of PharmacologyChina Pharmaceutical UniversityNanjing 210009China
出 版 物：《Journal of Molecular Cell Biology》 (分子细胞生物学报（英文版）)
年 卷 期：2022年第14卷第2期
页 面：43-55页
核心收录：
学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学]
基 金：supported by grants from the National Natural Science Foundation of China(81871937,82001586,91859204,and 82072629) CAMS Innovation Fund for Medical Sciences(CIFMS,2019-I2M-5-044) the Natural Science Foundation of Zhejiang Province(LZ21H160001) the China Postdoctoral Science Foundation(2021M692797)
主 题：colorectal cancer alternative splicing transcription elongation GLTSCR1
摘 要：Alternative splicing(AS)and transcription elongation are vital biological processes,and their dysregulation causes multiple diseases,including ***,the coregulatory mechanism of AS and transcription elongation in tumors remains *** study demonstrates a novel AS pattern of tight junction protein 1(ZO1)regulated by the RNA polymerase II elongation rate in colorectal cancer(CRC).Glioma tumor suppressor candidate region gene 1(GLTSCR1)decreases the transcription elongation rate of ZO1 to provide a time window for binding of the splicing factor HuR to the specific motif in intron 22 of ZO1 and spliceosome recognition of the weak 3 and 5 splice sites in exon 23 to promote exon 23 *** exon 23 inclusion in ZO1 suppresses migration and invasion of CRC cells,our findings suggest a novel potential therapeutic target for CRC.
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