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<p>Colorectal cancer (CRC) is a prevalent and highly lethal malignancy. RNA-binding motif (RBM) proteins have been demonstrated in CRC pathogenesis. However, the biological function and regulatory mechanisms of <i>RBM41</i> in CRC remain poorly understood. Here, we demonstrate that <i>RBM41</i> is significantly elevated in CRC tissues and is associated with poor prognosis in patients. Overexpression of RBM41 can enhance the malignant proliferation phenotype of CRC cells; in contrast, inhibition of <i>RBM41</i> significantly decreases CRC cell proliferation and induces autophagic cell death and apoptosis in HT29 and SW480 cells. Mechanistically, <i>RBM41</i> interferes with the processing of N-myc downregulated gene 1 (<i>NDRG1</i>) pre-mRNA by directly binding to its 3’ untranslated region (3’ UTR), thereby decreasing the mature transcript and protein levels of tumor suppressor <i>NDRG1</i>. Concurrent knockdown of <i>NDRG1</i> reversed the oncogenic functions of <i>RBM41</i> in HT29 cells and in fast-growing xenograft tumors in vivo. Moreover, patient-derived organoid (PDO) models with high <i>RBM41</i> expression exhibited increased resistance to 5-fluorouracil, oxaliplatin, and irinotecan. In summary, our findings demonstrate that <i>RBM41</i> promotes CRC progression by post-transcriptionally repressing <i>NDRG1</i>, underscoring its potential as a promising therapeutic target for CRC.</p>

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RNA binding motif protein RBM41 promotes colorectal tumorigenesis by impeding the maturation of NDRG1 pre-mRNA

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月20日

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  • Yanxin Liu,
  • Jianfeng Mu,
  • Jiming Yu,
  • Qirong Li,
  • Tiantian Li,
  • Qiang Feng,
  • Tong Sun,
  • Ke Sun,
  • Yang Hao,
  • Jinhai Yu,
  • Dongxu Wang

摘要

Colorectal cancer (CRC) is a prevalent and highly lethal malignancy. RNA-binding motif (RBM) proteins have been demonstrated in CRC pathogenesis. However, the biological function and regulatory mechanisms of RBM41 in CRC remain poorly understood. Here, we demonstrate that RBM41 is significantly elevated in CRC tissues and is associated with poor prognosis in patients. Overexpression of RBM41 can enhance the malignant proliferation phenotype of CRC cells; in contrast, inhibition of RBM41 significantly decreases CRC cell proliferation and induces autophagic cell death and apoptosis in HT29 and SW480 cells. Mechanistically, RBM41 interferes with the processing of N-myc downregulated gene 1 (NDRG1) pre-mRNA by directly binding to its 3’ untranslated region (3’ UTR), thereby decreasing the mature transcript and protein levels of tumor suppressor NDRG1. Concurrent knockdown of NDRG1 reversed the oncogenic functions of RBM41 in HT29 cells and in fast-growing xenograft tumors in vivo. Moreover, patient-derived organoid (PDO) models with high RBM41 expression exhibited increased resistance to 5-fluorouracil, oxaliplatin, and irinotecan. In summary, our findings demonstrate that RBM41 promotes CRC progression by post-transcriptionally repressing NDRG1, underscoring its potential as a promising therapeutic target for CRC.