Differences in Expression of Epithelial-Mesenchymal Transition (EMT) Induction Genes TGF-Β Pathway Transition in Colorectal Cancer Patients Non-Metastatic and Metastatic

Articles in Press

Document Type : Research Articles

Authors

1 Department of Biology, Faculty of Science and Mathematics, Universitas Riau, Indonesia.

2 Department of Biology, Faculty of Mathematics and Natural Sciences, Universitas Negeri Malang, Malang, Indonesia.

3 Department of Biomedical Sciences, Faculty of Medicine, Universitas Brawijaya, Malang, Indonesia.

4 Digestive Surgeon Division, Faculty of Medicine, Public Health, and Nursing, Universitas Gadjah Mada, Special Region of Yogyakarta, Indonesia.

Abstract

Objective: This research focuses on molecular screening of mRNA by targeting EMT regulator genes in the TGF-β/SMAD pathway to determine the difference in EMT mechanisms between non-metastatic and metastatic primary tumor cells. Methods: The method uses Real time/quantitative Polymerase Chain Reaction (RT-qPCR) to measure the expression levels of target genes in colon tissue samples from non-metastatic and metastatic patient groups. Differences in target gene expression between the two groups were analyzed using t-tests. Results: The results of this study show significance differences in the expression of EMT-inducing genes on the TGF-β/Smad pathway between non-metastatic colorectal cancer groups and metastases. TGF-β1 (p-value : 0.041), Smad2 (p-value : 0.020), Snail1 (p-value : 0.028), Twist1 (p-value : 0.036), and ZEB1 (p-value : 0.045) gene expression was higher in the metastatic tumor group. In contrast to these genes, the expression of the Smad4 (p-value : 0.022), E-cadherin (p-value : 0.036), and vimentin (p-value : 0.048) genes was lower in the metastatic tumor group. Conclusion: The observed alterations in gene expression related to EMT within the TGF-β/Smad pathway in metastatic colorectal cancer are likely associated with the partial processes of EMT and MET. These alterations may contribute to further metastatic potential and increase the malignancy of the cancer.

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Main Subjects

Asian Pacific Journal of Cancer Prevention

Articles in Press, Accepted Manuscript
Available Online from 12 September 2025

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History

  • Receive Date: 21 November 2024
  • Revise Date: 11 June 2025
  • Accept Date: 01 September 2025

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