ArticleThe Journal of clinical investigation2025
SOX9 suppresses colon cancer via inhibiting epithelial-mesenchymal transition and SOX2 induction.
Article in The Journal of clinical investigation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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
7 citing papers in PubMed.
- Article
- RILPL2 suppresses metabolic reprogramming and progression of cervical cancer by attenuating LDHA protein stability and inhibiting H3K18 lactylation.Cell death & disease · 2026Article
- Colorectal cancer pathogenesis, oncogenic signaling networks and targeted therapeutic advances.Molecular biomedicine · 2026Review
- Review
- A Trojan horse nanoplatform overcoming delivery barriers for targeted gene immunotherapy of colorectal cancer.Frontiers in bioengineering and biotechnology · 2026Article
- Medroxyprogesterone Acetate Inhibits Tumorigenesis in Mouse Models of Oviductal High-Grade Serous Carcinoma.Cancers · 2025Article
- Glycine attenuates sepsis-induced white matter injury by modulating gut microbiota.Frontiers in molecular biosciences · 2025Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
The Wnt/β-catenin pathway regulates expression of the SOX9 gene, which encodes sex-determining region Y-box (SOX) transcription factor 9, a differentiation factor and potential β-catenin regulator. Because APC tumor suppressor defects in approximately 80% of colorectal cancers (CRCs) activate the Wnt/β-catenin pathway, we studied SOX9 inactivation in CRC biology. Compared with effects of Apc inactivation in mouse colon tumors, combined Apc and Sox9 inactivation instigated more invasive tumors with epithelial-mesenchymal transition (EMT) and SOX2 stem cell factor upregulation. In an independent mouse CRC model with combined Apc, Kras, and Trp53 defects, Sox9 inactivation promoted SOX2 induction and distant metastases. About 20% of 171 human CRCs showed loss of SOX9 protein expression, which correlated with higher tumor grade. In an independent group of 376 patients with CRC, low SOX9 gene expression was linked to poor survival, earlier age at diagnosis, and increased lymph node involvement. SOX9 expression reductions in human CRC were linked to promoter methylation. EMT pathway gene expression changes were prominent in human CRCs with low SOX9 expression and in a mouse cancer model with high SOX2 expression. Our results indicate SOX9 has tumor suppressor function in CRC; its loss may promote progression, invasion, and poor prognosis by enhancing EMT and stem cell phenotypes.
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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.