Evidence map›Paper›PMID 41226455›Full record

ArticleInternational journal of molecular sciences2025

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

Mark Spivak, Moshe Pahmer, Dorna Delrahimnia, Tzuriel Sapir, David Shifteh

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Mark SpivakCollege of Medicine, SUNY Downstate Health Sciences University, Brooklyn, NY 11203, USA.
Moshe PahmerDepartment of Biology, Yeshiva College, Yeshiva University, New York, NY 10033, USA.ORCID 0000-0003-0155-8586
Dorna DelrahimniaCollege of Health Professions, Pace University, New York, NY 10038, USA.
Tzuriel SapirPerelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.ORCID 0000-0002-1689-2176
David ShiftehCollege of Medicine, SUNY Downstate Health Sciences University, Brooklyn, NY 11203, USA.ORCID 0000-0002-4108-4664

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Colorectal NeoplasmsMAP Kinase Signaling SystemPhosphatidylinositol 3-KinasesProtein-Arginine N-MethyltransferasesGene Expression Regulation, NeoplasticHumansProtein Interaction MapsSignal TransductionPhosphatidylinositol 3-KinasesPRMT5 protein, humanProtein-Arginine N-MethyltransferasesAKTCRCERKKRASMEKmTORPI3KPRMT5PTENRAF

Identifiers

PMID41226455
PMCPMC12609650

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.