Ciliatine-Induced Apoptosis in Colorectal Cancer Cells: Targeting PPARδ for Tumor Suppression

Overview

Colorectal cancer (CRC) is a leading cause of cancer-related deaths, and gut bacteria play a crucial role in its pathogenesis. Gut bacteria metabolize dietary substrates to produce various metabolites that can either promote or suppress CRC tumorigenesis. While many studies have focused on metabolites that promote CRC, less attention has been spent on studying metabolites that exhibit anti -cancer activity. Discovering such compounds could lead to novel therapeutics. In this study, Fusobacterium nucleatum and Escherichia coli supernatants that are high in ciliatine, a representative phosphonate, were shown to inhibit the growth of COLO205 cells, a CRC cell line. Extended analyses involving diverse CRC cell lines (COLO205, HCT116, HCT15, and KM20L2) underscore ciliatine's anti -growth and anti-proliferative impact across the CRC spectrum, without affecting control human umbilical vein endothelial cells. Further mechanistic studies using flow cytometry revealed that ciliatine induced CRC cell growth inhibition through apoptosis (programmed cell death) rather than necros is, concurrently arresting cells at the sub -G0/G1 phase. Structural modeling analysis suggested that ciliatine may impede CRC cell growth by binding to PPARδ. This discovery positions ciliatine as a hitherto unrecognized anti -cancer agent for CRC. The implications extend beyond a mere scientific revelati on, promising novel therapeutic strategies for CRC management. Envisaging interventions that modulate gut bacteria populations, incorporate ciliatine into dietary supplements, or develop ciliatine -based drug s opens new avenues in the pursuit of effective CRC treatment. This study not only contributes to the scientific discourse but may lead to a paradigm shift in approaching CRC therapeutics.

Competition history

• JSHS 2024 Category not listed

Resources

• National JSHS abstract book ↗

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