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Beyond ribosomal function:RPS6 deficiency suppresses cholangiocarcinoma cell growth by disrupting alternative splicing

引用

Acta Pharmaceutica Sinica B 2024年第9期14卷 3931-3948页

作者： Wenkang Fu Yanyan Lin Mingzhen Bai Jia Yao Chongfei Huang Long Gao Ningning Mi Haidong Ma Liang Tian Ping Yue Yong Zhang Jinduo zhang Yanxian Ren Liyun Ding Lunzhi Dai joseph wleung Jinqiu Yuan Wenhua Zhang Wenbo Meng The First School of Clinical Medicne Lanzhou UniversityLanzhou 730030China Department of General Surgery the First Hospital of Lanzhou UniversityLanzhou 730030China Key Laboratory of Biotherapy and Regenerative Medicine of Gansu Province the First Hospital of Lanzhou UniversityLanzhou 730000China School of Physical Science and Technology Lanzhou UniversityLanzhou 730000China National Clinical Research Center for Geriatrics and Department of General Practice State Key Laboratory of BiotherapyWest China HospitalSichuan UniversityChengdu 610041China Division of Gastroenterology UC Davis Medical Center and Sacramento VA Medical CenterSacramentoCA 95817USA Clinical Research Center Big Data Centerthe Seventh Affiliated HospitalSun Yat-sen UniversityShenzhen 518107China School of Life Sciences Lanzhou UniversityLanzhou 730000China

Cholangiocarcinoma(CCA)is a bile duct malignancy with a dismal *** study systematically investigated the role of the ribosomal protein S6(RPS6)gene,which is dependent in *** found that RPS6 upregulation in CCA tissues was correlated with a poor *** investigations have shown that alterations in RPS6 expression,both gain-and loss-of function could affect the proliferation of CCA *** xenograft tumor models,RPS6 overexpression enhances tumorigenicity,whereas RPS6 silencing reduces *** analysis using RNA-seq and proteomics elucidated downstream signaling pathways of RPS6 depletion by affecting the cell cycle,especially DNA *** followed by mass spectrometry has identified numerous spliceosome complex proteins associated with *** profiling revealed that RPS6 affects numerous alternative splicing(AS)events,and combined with RNA immunoprecipitation sequencing,revealed that minichromosome maintenance complex component 7(MCM7)binds to RPS6,which regulates its AS and increases oncogenic activity in *** RPS6 with vivo phosphorodiamidate morpholino oligomer(V-PMO)significantly inhibited the growth of CCA cells,patient-derived organoids,and subcutaneous xenograft *** together,the data demonstrate that RPS6 is an oncogenic regulator in CCA and that RPS6-V-PMO could be repositioned as a promising strategy for treating CCA.

关键词： Cholangiocarcinoma Ribosomal protein S6 Alternative splicing p53 Minichromosome maintenance complex component 7 Vivo morpholino Patient-derived organoids

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