ArticleCell death & disease2025
USP14/S100A11 axis promote colorectal cancer progression by inhibiting cell senescence.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Article
- S100A10 promotes tumorigenesis and metastasis in lung adenocarcinoma by regulating JUND/TNC axis-mediated EMT.Translational oncology · 2026Article
- Lactylation-driven stabilization of the S100A11/ANXA2 complex promotes pancreatic cancer metastasis.Cell biology and toxicology · 2026Article
- Emerging regulatory model of Ubiquitin-Specific Proteases 14 in cancer: from canonical oncogenesis to TME modulation, therapeutic resistance, and non-canonical activities.Journal of translational medicine · 2026Review
- Macrophage-derived IL-6 reprograms lipid metabolism to promote colorectal cancer development through USP14-mediated FASN deubiquitination.Journal of translational medicine · 2026Article
- USP14 promotes epithelial-mesenchymal transition and functions as a multifaceted biomarker in lung adenocarcinoma.Discover oncology · 2026Article
- Bioinformatics combined with machine learning for the identification of malignant transformation markers in colorectal polyps.Frontiers in molecular biosciences · 2026Article
- Unveiling the protein landscape for early detection of colorectal precancerous lesions.Clinical proteomics · 2025Article
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aberrant expression of S100A11 has been identified in various malignancies but its functional roles and underlying mechanisms in colorectal cancer (CRC) have not been fully elucidated. Therefore, this study was designed to investigate the expression of S100A11 and its functional significance in CRC, indicating that S100A11 is significantly upregulated and correlates with poor survival outcomes in CRC. Functionally, S100A11 knockdown in CRC cell lines inhibited cell proliferation, invasion, and migration, leading to decreased tumour growth and metastasis in vivo. Mechanistic investigations revealed that S100A11 promotes cell proliferation and invasion by suppressing cell senescence. In addition, USP14 interacts with and mediates S100A11 deubiquitination. More importantly, the overexpression of S100A11 was able to partially counteract the reduction in cell proliferation caused by the knockdown of USP14. In summary, the novel regulatory axis involving USP14 and S100A11 modulates the malignant biological behavior of CRC cells through inhibiting cell senescence, therefore the interaction between USP14 and S100A11 represents a promising therapeutic target in 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 OpenQuestion graph.