5-Azacytidine Reactivates E-cadherin via Promoter Demethylation and Induces Autophagy in Colorectal Cancer Cells

Document Type : Original Article

Authors

1 Department of Biological Sciences, Faculty of Science, King Abdulaziz University, Jeddah, Saudi Arabia

2 Princess Doctor Najla Bint Saud Al Saud Distinguished Research Centre for Biotechnology, King Abdulaziz University, Jeddah, Saudi Arabia

Abstract

Colorectal cancer (CRC) is a severe neoplasm that is associated with high mortality rates. Aberrant epigenetic alterations are associated with several stages of tumor growth. The FDA has approved 5-Azacytidine (5-aza) for the treatment of specific types of cancers, including leukemia and MDS. Previous studies have demonstrated that E-cadherin1 (CDH1) expression is suppressed in CRC. However, the regulatory mechanisms underlying CDH1 suppression remain unclear. This investigation focused on examining whether 5-aza has a significant effect on CRC treatment using the human LS513 cell line. MTT test was used to evaluate the LS513 cell viability following 5-aza treatment; cell proliferation along with autophagy were assessed using flow cytometry; CDH1 expression was analyzed by quantitative reverse transcription polymerase chain reaction (RT-qPCR) and Western blotting, while methylation-specific PCR (MSP-PCR) was used to investigate the degree of methylation in the CDH1 promoter region. These Findings indicate that 5-aza reduced the viability of LS513 cells in a concentration-dependent manner (P < 0.05). 5-aza treatment arrested the cell cycle at the G2/M phase, triggered autophagy, and upregulated CDH1 expression following deactivation of the hypermethylated CDH1 promoter.

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History

  • Receive Date: 30 August 2025
  • Revise Date: 16 October 2025
  • Accept Date: 29 October 2025

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