ArticleMedComm2025
Prolyl 4-hydroxylase α-subunit family regulation of type I collagen deposition and IL17RB/c-Jun activation synergistically mediate choline dehydrogenase promotion of colorectal cancer metastasis.
Article in MedComm, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
5 citing papers in PubMed.
- Enhanced Collagen Prolyl 4-Hydroxylase Activity and Expression Promote Cancer Progression via Both Canonical and Non-Canonical Mechanisms.International journal of molecular sciences · 2025Review
- CHDH Promotes Breast Cancer Metastasis Relying on IL17RB/CREB1 Signalling Activation.Journal of cellular and molecular medicine · 2025Article
- Constructing a mitochondrial-related genes model based on machine learning for predicting the prognosis and therapeutic effect in colorectal cancer.Discover oncology · 2025Article
- Article
- Organotropic metastasis in colorectal cancer: integrating molecular pathways with therapeutic opportunities.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metastasis continues to pose a significant challenge in tumor treatment. Evidence indicates that choline dehydrogenase (CHDH) is crucial in tumorigenesis. However, the functional role of CHDH in colorectal cancer (CRC) metastasis remains unreported. The study explored the functional role and mechanism of CHDH in CRC metastasis using human CRC tissues and a xenograft mouse model. CHDH expression was significantly higher in CRC compared to normal tissues and showed a positively correlation with CRC tumor-nodes-metastasis stage. CRC cell lines showed increased CHDH expression compared to normal controls. CHDH knockdown suppressed cell migration in vitro and tumor metastasis in vivo. Similarly, ectopic CHDH expression enhanced cell migration in vitro and tumor metastasis in vivo. Results suggested that CHDH affected the histone H3 trimethylation levels, which upregulated prolyl 4-hydroxylase α-subunit (P4HA) family gene (P4HA1/2/3) expression, further stabilizing collagen I expression and increasing IL17RB expression, which promoted downstream c-Jun activation. Together, P4HA and IL17RB promote CRC cell metastasis. P4HA and c-Jun inhibitors abolished CHDH-mediated CRC cell metastasis in vitro and in vivo. Collectively, the above findings provide novel evidence that that CHDH mediates CRC cell metastasis and may be a promising target for metastatic CRC therapy.
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