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<p>Colorectal cancer (CRC) progression critically depends on the tumor microenvironment. PLOD2, an enzyme involved in collagen biosynthesis, is highly expressed in many cancers. While it promotes CRC growth via the USP15–AKT/mTOR pathway, its role in enhancing tumor cell migration and invasion remains unclear. Our study identified a significant upregulation of PLOD2 in colorectal cancer. This upregulation was closely associated with clinical stage, lymph node metastasis, and nerve invasion in CRC. Functional assays, including CCK-8, colony formation, wound healing, and Transwell migration and invasion assays, showed that PLOD2 overexpression enhanced CRC cell proliferation, migration, and invasion, while PLOD2 silencing exerted the opposite effects. Kyoto Encyclopedia of Genes and Genomes pathway analysis suggested that PLOD2 may influence CRC progression via the PI3K-AKT signaling pathway. Co-immunoprecipitation assays demonstrated that PLOD2 was co-precipitated with PI3K, confirming their interaction. Additionally, rescue experiments showed that the PI3K inhibitor LY294002 and the agonist 740Y-P could reverse PLOD2-mediated effects on CRC cell proliferation, migration, and invasion. This study demonstrates that PLOD2 promotes the proliferation, migration, and invasion of CRC cells by interacting with PI3K to activate the PI3K-AKT-GSK3β signaling pathway.</p>

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PLOD2 promotes proliferation, migration and invasion of colorectal cancer cells via PI3K-AKT-GSK3β signaling pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月10日

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  • Hua Fang,
  • Jing Zheng,
  • Shutong Ren,
  • Danjing Chen,
  • Yunli Wu,
  • Xian-E Peng

摘要

Colorectal cancer (CRC) progression critically depends on the tumor microenvironment. PLOD2, an enzyme involved in collagen biosynthesis, is highly expressed in many cancers. While it promotes CRC growth via the USP15–AKT/mTOR pathway, its role in enhancing tumor cell migration and invasion remains unclear. Our study identified a significant upregulation of PLOD2 in colorectal cancer. This upregulation was closely associated with clinical stage, lymph node metastasis, and nerve invasion in CRC. Functional assays, including CCK-8, colony formation, wound healing, and Transwell migration and invasion assays, showed that PLOD2 overexpression enhanced CRC cell proliferation, migration, and invasion, while PLOD2 silencing exerted the opposite effects. Kyoto Encyclopedia of Genes and Genomes pathway analysis suggested that PLOD2 may influence CRC progression via the PI3K-AKT signaling pathway. Co-immunoprecipitation assays demonstrated that PLOD2 was co-precipitated with PI3K, confirming their interaction. Additionally, rescue experiments showed that the PI3K inhibitor LY294002 and the agonist 740Y-P could reverse PLOD2-mediated effects on CRC cell proliferation, migration, and invasion. This study demonstrates that PLOD2 promotes the proliferation, migration, and invasion of CRC cells by interacting with PI3K to activate the PI3K-AKT-GSK3β signaling pathway.