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The Role of ULK3 in Cancer Progression: A Pan-Cancer Bioinformatics Analysis Integrated with Experimental Validation
Yangyang Han1,2,3, Mengqi Zhang1, Mannizire Rehemujiang1
1Department of Biology, School of Basic Medical Sciences, Xinjiang Medical University, Urumqi 830017, China.
International Journal of Molecular Sciences
|July 15, 2026
Summary
Unc-51-like kinase 3 (ULK3) is upregulated in many cancers, correlating with poor outcomes and immune suppression. This study reveals ULK3’s potential as a pan-cancer biomarker and immunotherapy predictor.
Area of Science:
- Oncology
- Molecular Biology
- Genomics
Background:
- Unc-51-like kinase 3 (ULK3) is a serine/threonine kinase implicated in tumorigenesis.
- The exact role of ULK3 in cancer initiation and progression requires further elucidation.
Purpose of the Study:
- To comprehensively analyze ULK3 expression, genomic alterations, and functional roles across 33 cancer types.
- To investigate the prognostic significance, immune infiltration, and therapeutic potential of ULK3.
Main Methods:
- Integrated analysis of multi-omics data from TCGA, GTEx, and CPTAC for transcript and protein levels.
- Evaluation of genomic alterations, alternative splicing, pathway enrichment, and tumor stemness.
- Functional assays in prostate cancer cells (PC-3) and drug screening using Connectivity Map.
Main Results:
- ULK3 was upregulated in 13 cancers (e.g., Bladder, Breast, Lung) and downregulated in 2 (e.g., Cholangiocarcinoma).
- High ULK3 expression correlated with poor survival in specific cancers and was linked to copy number amplification and mutations.
- ULK3 dysregulation was associated with tumor stemness, altered RNA modifications, immune suppression (M2 macrophages, PD-L1, CTLA4), and TMB/MSI.
Conclusions:
- ULK3 expression and amplification are linked to adverse clinical outcomes, tumor stemness, and immune evasion across multiple cancers.
- ULK3 serves as a potential pan-cancer diagnostic and prognostic biomarker.
- ULK3 may predict immunotherapy response, particularly in prostate cancer, where its activator Cephaeline was identified.
