ArticleBMC cancer2025
A Multi-PTM omics atlas uncovers novel aging regulators in colorectal cancer.
Article in BMC cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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.
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Who cites it
3 citing papers in PubMed.
- Combinatorial post-translational modification reprogramming of the endomembrane system in colorectal cancer.Translational cancer research · 2026Article
- Precision Profiling of the Cardiovascular Post-Translationally Modified Proteome.Journal of cardiovascular development and disease · 2026Review
- A Multi-omics PTM Atlas Reveals Key Insights into Metabolic Reprogramming in Colorectal Cancer.Cancer genomics & proteomicsArticle
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
backgroundAging is a key driver of colorectal cancer (CRC) progression, yet the post-translational modification (PTM) landscape associated with aging in CRC remains largely uncharacterized. In particular, the coordinated influence of multiple PTMs-such as phosphorylation, ubiquitination, and malonylation-on aging-related pathways has not been systematically explored.
methodsIn this study, we established a CRC-specific multiomics framework by profiling phosphorylation, malonylation, and ubiquitination in matched tumor and adjacent normal tissues (n = 8 pairs). The differentially modified proteins were subjected to functional enrichment, protein-protein interaction (PPI) network construction, structural mapping, and aging pathway annotation. Key regulatory axes were reconstructed through integration of GO, KEGG, and literature-based evidence.
resultsAging-related PTMs were extensively dysregulated in CRC, with 162 ubiquitination sites, 64 phosphorylation sites, and 68 malonylation sites altered. LMNB1 has emerged as a multi-PTM protein, indicating coordinated control of the nuclear structure during senescence. PPI network analysis highlighted CDK1, SOD2, and MAPK1 as potential hub PTM-regulated nodes involved in the aging program of CRC. An integrated signaling model further demonstrated how PTM-mediated suppression of the EGFR-RAS axis, along with activation of the p38 and p53 pathways, collectively contributes to shaping the aging phenotype in CRC.
conclusionThis study presents the first integrative network map of aging regulation in CRC based on multiple PTMs. Notably, hub proteins such as LMNB1 have emerged as key regulatory targets. These findings provide a theoretical foundation for the development of aging-cancer axis-related biomarkers and therapeutic strategies for CRC.
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Registered trials
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.