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Objective <p>This study aimed to investigate the biological function and the molecular mechanism of ENDOD1 in colorectal cancer (CRC) progression.</p> Methods <p>CRC-related differentially expressed genes (DEGs) were screened by analyzing GEO datasets (GSE41657, GSE8671, GSE41328, and GSE75548). The differential expression of ENDOD1 within human CRC cell lines (HCT116, HT-29, SW620, and SW480) versus human normal colonic epithelial cells (NCM460) was validated using RT-qPCR and Western blot. ENDOD1 overexpression vector and siRNA were constructed and transfected into HT29 cells. CCK-8, flow cytometry, scratch test, and Transwell assays were performed to assess HT29 cell viability, apoptosis, and migratory and invasive abilities. The regulatory role of ENDOD1 in tumor growth in vivo was investigated using a xenograft mouse model. Moreover, a Western blot was performed to determine Wnt/β-catenin signaling activation.</p> Results <p>ENDOD1 was down-regulated in CRC tissues of GSE41657, GSE8671, GSE41328, and GSE75548 datasets, as well as in CRC cell lines. ENDOD1 overexpression promoted HT29 cell apoptosis and suppressed cell viability, migration, and invasion; ENDOD1 downregulation suppressed HT29 cell apoptosis and enhanced cell viability, migration, and invasion. In vivo, ENDOD1 overexpression inhibited tumor growth, suppressed Ki67 expression, and promoted apoptosis in transplanted tumors in mice. Moreover, EMDOD1 overexpression was blocked, while ENDOD1 inhibition promoted the activation of the Wnt/β-catenin pathway. Pharmacological activation of the Wnt/β‑catenin pathway partially attenuated ENDOD1-mediated suppression in CRC cells.</p> Conclusion <p>ENDOD1 expression level is decreased in CRC, and overexpression of ENDOD1 induces apoptosis, represses cell proliferation, migratory and invasive ability, and inhibits the Wnt/β-catenin signaling activation within CRC cells.</p>

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Overexpression of ENDOD1 inhibits proliferation, migration, and invasion of colorectal cancer

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月26日

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  • Yichi Zhang,
  • Nijina Li,
  • Hao Zhang,
  • Dehua Hu

摘要

Objective

This study aimed to investigate the biological function and the molecular mechanism of ENDOD1 in colorectal cancer (CRC) progression.

Methods

CRC-related differentially expressed genes (DEGs) were screened by analyzing GEO datasets (GSE41657, GSE8671, GSE41328, and GSE75548). The differential expression of ENDOD1 within human CRC cell lines (HCT116, HT-29, SW620, and SW480) versus human normal colonic epithelial cells (NCM460) was validated using RT-qPCR and Western blot. ENDOD1 overexpression vector and siRNA were constructed and transfected into HT29 cells. CCK-8, flow cytometry, scratch test, and Transwell assays were performed to assess HT29 cell viability, apoptosis, and migratory and invasive abilities. The regulatory role of ENDOD1 in tumor growth in vivo was investigated using a xenograft mouse model. Moreover, a Western blot was performed to determine Wnt/β-catenin signaling activation.

Results

ENDOD1 was down-regulated in CRC tissues of GSE41657, GSE8671, GSE41328, and GSE75548 datasets, as well as in CRC cell lines. ENDOD1 overexpression promoted HT29 cell apoptosis and suppressed cell viability, migration, and invasion; ENDOD1 downregulation suppressed HT29 cell apoptosis and enhanced cell viability, migration, and invasion. In vivo, ENDOD1 overexpression inhibited tumor growth, suppressed Ki67 expression, and promoted apoptosis in transplanted tumors in mice. Moreover, EMDOD1 overexpression was blocked, while ENDOD1 inhibition promoted the activation of the Wnt/β-catenin pathway. Pharmacological activation of the Wnt/β‑catenin pathway partially attenuated ENDOD1-mediated suppression in CRC cells.

Conclusion

ENDOD1 expression level is decreased in CRC, and overexpression of ENDOD1 induces apoptosis, represses cell proliferation, migratory and invasive ability, and inhibits the Wnt/β-catenin signaling activation within CRC cells.