A Further Case for Targeting PRMT5 and the ERK1/2 and PI3K Pathways in CRC

TL;DR

This paper argues for targeting PRMT5 and two key cancer pathways to improve colorectal cancer treatment.

Contribution

The study provides new evidence of PRMT5's interaction with ERK1/2 and PI3K pathways in colorectal cancer.

Findings

PRMT5 is positively correlated with ERK1/2 and PI3K pathways in CRC.

PRMT5 interacts with ERK1/2 and PI3K pathways based on protein–protein interaction networks.

The findings support the need for therapies targeting PRMT5 and these pathways in CRC.

Abstract

Colorectal cancer (CRC) is the second leading cause of cancer-related mortality in the United States. Recent breakthroughs in research are highlighting the complex genetic and epigenetic alterations driving CRC progression. Among these, the ERK1/2 and PI3K pathways are central regulators of cellular proliferation, survival, and differentiation. The overactivation of these pathways is frequently observed in cancer and is associated with poor patient prognosis. Protein Arginine Methyltransferase 5 (PRMT5), a key epigenetic regulator, has been implicated in modulating the ERK1/2 and PI3K pathways in cancer. Previous studies, including those from our own group, are starting to suggest that targeting PRMT5 and the ERK1/2 and PI3K pathways may offer therapeutic benefits. Thus, we sought to provide further evidence of the relationship between PRMT5 and the ERK1/2 and PI3K pathways in CRC. Using patient tumor gene expression data and protein–protein interaction networks, we provide further evidence that PRMT5 is positively correlated with, and interacts with, the ERK1/2 and PI3K pathways in CRC. These findings are significant, as they further strengthen the case for the urgent need of additional research into therapeutic strategies targeting PRMT5 and the ERK1/2 and PI3K pathways in CRC.

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