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<p>Neurochondrin (NCDN) has been recently identified as overexpressed in liver metastatic colorectal cancer (CRC) cells compared to poorly metastatic isogenic counterparts. While its cellular function and role in cancer and CRC remain unknown, patient survival data indicate that elevated NCDN levels are associated with poor prognosis. After validating these observations in an independent patient cohort, we sought to investigate the role of NCDN in CRC progression using isogenic CRC cell models comprising poorly metastatic KM12C and liver-metastatic KM12SM cells, and poorly metastatic SW480 and lymph node-metastatic SW620 cells. Stable silencing of NCDN expression in these cell lines resulted in a significant reduction in their tumorigenic and metastatic properties in vitro. Furthermore, in vivo assays using nude mice and the KM12 cell model demonstrated that NCDN is essential for tumor initiation, growth, and liver metastasis of CRC cells. Proteomic profiling of NCDN-silenced cells uncovered a set of dysregulated proteins associated with cell adhesion, invasion, cell death, and differentiation, and mitochondrial dysfunction, emerging NCDN-PODXL-EZR axis as a critical mediator of CRC progression and involved in liver metastasis. Our findings position NCDN and their associated dysregulated proteins as drivers of CRC progression and promising targets for further investigation.</p>

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Neurochondrin drives colorectal cancer progression by modulating the PODXL–Ezrin axis and mitochondrial function

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年4月17日

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  • María Garranzo-Asensio,
  • Elisa Carral-Ibarra,
  • Ana Montero-Calle,
  • Marta Gómez de Cedrón,
  • Javier Velázquez-Gutiérrez,
  • Susana Molina,
  • Jana Dziakova,
  • Rodrigo Sanz-López,
  • Carmen Povès,
  • Ana Ramírez de Molina,
  • Javier Martínez-Useros,
  • María Jesús Fernández-Aceñero,
  • Rubén A. Bartolomé,
  • Rodrigo Barderas

摘要

Neurochondrin (NCDN) has been recently identified as overexpressed in liver metastatic colorectal cancer (CRC) cells compared to poorly metastatic isogenic counterparts. While its cellular function and role in cancer and CRC remain unknown, patient survival data indicate that elevated NCDN levels are associated with poor prognosis. After validating these observations in an independent patient cohort, we sought to investigate the role of NCDN in CRC progression using isogenic CRC cell models comprising poorly metastatic KM12C and liver-metastatic KM12SM cells, and poorly metastatic SW480 and lymph node-metastatic SW620 cells. Stable silencing of NCDN expression in these cell lines resulted in a significant reduction in their tumorigenic and metastatic properties in vitro. Furthermore, in vivo assays using nude mice and the KM12 cell model demonstrated that NCDN is essential for tumor initiation, growth, and liver metastasis of CRC cells. Proteomic profiling of NCDN-silenced cells uncovered a set of dysregulated proteins associated with cell adhesion, invasion, cell death, and differentiation, and mitochondrial dysfunction, emerging NCDN-PODXL-EZR axis as a critical mediator of CRC progression and involved in liver metastasis. Our findings position NCDN and their associated dysregulated proteins as drivers of CRC progression and promising targets for further investigation.