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<p>Colorectal cancer (CRC) is one of the most common tumors worldwide, and metastatic CRC is likely to have a poor prognosis. N7-methylguanosine (m7G) is a common methylation modification that is catalyzed primarily by methyltransferase 1 (METTL1). However, the role of m7G in metastatic CRC remains unclear. The role of METTL1 in progressive CRC was initially explored using bioinformatics analysis. Subsequently, its relationship with CRC was further validated through in vitro and in vivo experiments. Potential downstream targets were identified through RNA-seq and quantitative real-time PCR (RT‒qPCR), and the underlying mechanisms were investigated using methylated RNA immunoprecipitation (MeRIP) and RNA degradation assays. Our results revealed that METTL1 is differentially expressed and significantly upregulated in metastatic CRC. This correlation was further confirmed by in vivo and in vitro experiments. RNA sequencing of CRC cells with METTL1 knockdown revealed that intercellular adhesion molecule-1 (ICAM-1) was a significant downstream target and could be stabilized by m7G modification. We revealed that METTL1 is significantly upregulated in metastatic CRC and plays a critical role in CRC progression by stabilizing ICAM-1 through m7G modification.</p>

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METTL1-mediated m7G modification promotes colorectal cancer metastasis via stabilization of ICAM-1

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年4月19日

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  • Shangwen Cai,
  • Shuyi Mi,
  • Jingyu Chen,
  • Liming Shao,
  • Xiaoyun Yang,
  • Meng Xue

摘要

Colorectal cancer (CRC) is one of the most common tumors worldwide, and metastatic CRC is likely to have a poor prognosis. N7-methylguanosine (m7G) is a common methylation modification that is catalyzed primarily by methyltransferase 1 (METTL1). However, the role of m7G in metastatic CRC remains unclear. The role of METTL1 in progressive CRC was initially explored using bioinformatics analysis. Subsequently, its relationship with CRC was further validated through in vitro and in vivo experiments. Potential downstream targets were identified through RNA-seq and quantitative real-time PCR (RT‒qPCR), and the underlying mechanisms were investigated using methylated RNA immunoprecipitation (MeRIP) and RNA degradation assays. Our results revealed that METTL1 is differentially expressed and significantly upregulated in metastatic CRC. This correlation was further confirmed by in vivo and in vitro experiments. RNA sequencing of CRC cells with METTL1 knockdown revealed that intercellular adhesion molecule-1 (ICAM-1) was a significant downstream target and could be stabilized by m7G modification. We revealed that METTL1 is significantly upregulated in metastatic CRC and plays a critical role in CRC progression by stabilizing ICAM-1 through m7G modification.