Evidence map›Paper›PMID 41009603›Full record

ReviewInternational journal of molecular sciences2025

Therapeutic Targeting of Protein Lysine and Arginine Methyltransferases: Principles and Strategies for Inhibitor Design.

Isaac Micallef, Byron Baron

Abstract readReview
In one paragraph

Review 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. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
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

2 authors.

Isaac MicallefDepartment of Tumor Genetics and Biology, Graduate School of Medical Sciences, Faculty of Life Sciences, Kumamoto University, Kumamoto 860-8556, Japan.ORCID 0000-0002-4602-1400
Byron BaronCentre for Molecular Medicine and Biobanking, University of Malta, MSD 2080 Msida, Malta.ORCID 0000-0001-5722-6295

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Standard cancer chemotherapy is increasingly being supplemented with novel therapeutics to overcome known chemoresistance pathways. Resistance to treatment is common across various tumour types, driven by multiple mechanisms. One emerging contributor is protein methylation, a post-translational modification mediated by protein methyltransferases (PMTs), which regulate protein function by adding methyl groups, mainly on lysine and arginine residues. Dysregulation of protein lysine methyltransferases (PKMTs) and protein arginine methyltransferases (PRMTs) has been linked to cancer progression and drug resistance, making them attractive therapeutic targets. Consequently, several small-molecule PMT inhibitors have been developed, with some progressing to clinical trials. However, many candidates showing promise in preclinical studies fail to demonstrate efficacy or safety in later stages, limiting clinical success. This gap highlights the need to rethink current approaches to PMT inhibitor design. A deeper understanding of PMT mechanisms, catalytic domains, and their roles in chemoresistance is essential for creating more selective, potent, and clinically viable inhibitors. This review will summarise major chemoresistance pathways and PMTs implicated in cancer, then explore current and prospective PMT inhibitor classes. Building on mechanistic insights, we propose strategies to develop next-generation inhibitors with improved therapeutic potential against chemoresistant cancers.

Indexed as

Antineoplastic AgentsEnzyme InhibitorsHistone-Lysine N-MethyltransferaseNeoplasmsProtein-Arginine N-MethyltransferasesAnimalsDrug DesignDrug Resistance, NeoplasmHumansMolecular Targeted TherapyProtein Processing, Post-TranslationalAntineoplastic AgentsEnzyme InhibitorsHistone-Lysine N-MethyltransferaseProtein-Arginine N-MethyltransferaseschemoresistancemethylproteomicsPMT inhibitorsprotein methylationprotein methyltransferases (PMTs)

Identifiers

PMID41009603
PMCPMC12469536

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.