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<p>Cancer stem cells were prominent responsible for cancer initiation, metastasis, and invasion as well as therapeutic resistance in colorectal cancer (CRC). The extracellular axon guidance factor netrin-1 has been found to be overexpressed in several malignant cancers such as glioma, lung cancers, and colorectal cancer. However, the role of netrin-1 on cancer stemness in CRC remains unveiled. Our study revealed high expression of netrin-1 in colorectal cancer tissues and its ability to promote cancer stemness by interacting with receptors UNC5B and neogenin on murine colorectal cancer cell. Mechanistically, the netrin-1-UNC5B/neogenin axis activates the downstream NF-κB and ERK1/2 signaling pathways, reinforcing the stemness properties of tumor cells, and further exacerbating tumor progression. Clinically, netrin-1 expression associated with poor survival and high CD133 expression in patients with CRC. Taken together, these results suggest that netrin-1 blockade could be a compelling therapeutic strategy to improve the poor outcomes and trigger cancer stemness inhibition in CRC treatment.</p>

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Netrin-1-UNC5B/neogenin axis enhances the stemness of colorectal cancer cells

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月13日

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  • Xueli Xia,
  • Zhenwei Mao,
  • Wenxin Wang,
  • Lin Zhao,
  • Mengxue Xu,
  • Jie Ma,
  • Jie Tian,
  • Kai Yin,
  • Shengjun Wang

摘要

Cancer stem cells were prominent responsible for cancer initiation, metastasis, and invasion as well as therapeutic resistance in colorectal cancer (CRC). The extracellular axon guidance factor netrin-1 has been found to be overexpressed in several malignant cancers such as glioma, lung cancers, and colorectal cancer. However, the role of netrin-1 on cancer stemness in CRC remains unveiled. Our study revealed high expression of netrin-1 in colorectal cancer tissues and its ability to promote cancer stemness by interacting with receptors UNC5B and neogenin on murine colorectal cancer cell. Mechanistically, the netrin-1-UNC5B/neogenin axis activates the downstream NF-κB and ERK1/2 signaling pathways, reinforcing the stemness properties of tumor cells, and further exacerbating tumor progression. Clinically, netrin-1 expression associated with poor survival and high CD133 expression in patients with CRC. Taken together, these results suggest that netrin-1 blockade could be a compelling therapeutic strategy to improve the poor outcomes and trigger cancer stemness inhibition in CRC treatment.