ArticleDiscover oncology2025
Integrated multi-omics analysis reveals PTM networks as key regulators of colorectal cancer progression and immune evasion.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Precision Profiling of the Cardiovascular Post-Translationally Modified Proteome.Journal of cardiovascular development and disease · 2026Review
- Exercise-specific post-translational modification signatures: unveiling precise regulatory mechanisms of molecular exercise language and cellular adaptation.Frontiers in sports and active living · 2026Review
- PTM encoding: decoding the mechanisms of exercise-induced metabolic memory through spatiotemporal modification networks.Frontiers in sports and active living · 2026Review
- Integrated multi-omics characterization of SPTBN2 overexpression reveals its pro-tumorigenic role and immune microenvironment remodeling in colorectal cancer.Frontiers in cell and developmental biology · 2026Article
- GalNAc-Transferases in Cancer.Biomedicines · 2025Review
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Authors and funding
8 authors.
Funding
Abstract
backgroundColorectal cancer (CRC) is a leading cause of cancer mortality, with treatment resistance often driven by molecular heterogeneity and an immunosuppressive tumor microenvironment (TME). Post-translational modifications (PTMs) regulate key oncogenic processes, but their comprehensive role in CRC progression and immune evasion remains unexplored.
methodsWe integrated multi-omics data from bulk RNA-seq (GEO/TCGA, n = 1,783), single-cell transcriptomics (41,143 cells), and Mendelian randomization. Differential expression, GSVA, and machine learning (LASSO/SVM/Random Forest) were used to identify PTM-associated signatures. Functional validation included spatial transcriptomics, and immune profiling.
resultsMulti-omics analysis identified dysregulation in 80% of PTM pathways in CRC, with ubiquitination sustaining Wnt/β-catenin signaling and GALNT6-mediated glycosylation driving immune evasion through PD-L1 stabilization and CD8 + T cell exclusion. Single-cell analysis revealed GALNT6-specific enrichment in immune-excluded goblet cells (p < 0.05). Machine learning derived a 5-gene PTM Activity Signature (CCNB1IP1, GALNT6, NEDD4L, PSMD14, UBE2C) that distinguish between patients with diseases and those without (AUC = 1.00). GALNT6 was validated as a causal risk factor (OR = 1.10, 95%CI:1.01-1.18), with its inhibition synergizing with anti-PD-1 to enhance CD8 + T cell infiltration (p < 0.01).
conclusionThis study establishes PTM networks as central regulators of CRC progression and immune resistance. The PTM-AS framework enables precision subtyping, while GALNT6 emerges as a novel therapeutic target for overcoming immunotherapy resistance.
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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 Socratic graph.