ArticleInternational journal of cancer2025
14-3-3σ restricts YY1 to the cytoplasm, promoting therapy resistance, and tumor progression in colorectal cancer.
Article in International journal of cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Stress-specific 14-3-3-client modules in digestive cancers: an evidence-graded review of adaptive survival and therapy resistance.Cancer biology & therapy · 2026Review
- Mechanisms and advances of drug resistance in colorectal cancer: A systematic overview of multi-layered regulatory networks.Translational oncology · 2026Review
- Exploring 14-3-3ζ: insights into its role in cancer mechanisms and future therapeutic applications.Hereditas · 2026Review
- Isoform-resolved 14-3-3/YWHA networks in colorectal cancer: phospho-adaptor mechanisms, biomarker contexts and therapeutic opportunities.Frontiers in oncology · 2026Review
- The Importance of 14-3-3 Proteins in Colorectal Cancer Regulation: Mechanisms of Function and Clinical Opportunities.BioMed research international · 2026Review
- Role and clinical significance of the DNA methylation of 14-3-3σ in cancer (Review).Oncology letters · 2025Review
- 14-3-3σ restricts YY1 to the cytoplasm, promoting therapy resistance, and tumor progression in colorectal cancer.International journal of cancer · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
14-3-3σ functions as an oncogene in colorectal cancer and is associated with therapy resistance. However, the mechanisms underlying these observations are not clear. The results in this report demonstrate that loss of 14-3-3σ in colorectal cancer cells leads to a decrease in tumor formation and increased sensitivity to chemotherapy. The increased sensitivity to chemotherapy is due to a decrease in the expression of UPR pathway genes in the absence of 14-3-3σ. 14-3-3σ promotes expression of the UPR pathway genes by binding to the transcription factor YY1 and preventing the nuclear localization of YY1. YY1, in the absence of 14-3-3σ, shows increased nuclear localization and binds to the promoter of the UPR pathway genes, resulting in decreased gene expression. Similarly, a YY1 mutant that cannot bind to 14-3-3σ also shows increased nuclear localization and is enriched on the promoter of the UPR pathway genes. Finally, inhibition of the UPR pathway with genetic or pharmacological approaches sensitizes colon cancer cells to chemotherapy. Our results identify a novel mechanism by which 14-3-3σ promotes tumor progression and therapy resistance in colorectal cancer by maintaining UPR gene expression.
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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.