ArticleThe Journal of biological chemistry2025
HKDC1 promotes colorectal cancer progression by regulating RCOR1 expression to activate the Wnt/β-catenin pathway, enhancing proliferation, migration, and epithelial-mesenchymal transition.
Article in The Journal of biological chemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Epigenetic reprogramming of hexokinase domain containing 1 (HKDC1) promotes proliferation in colorectal cancer.American journal of cancer research · 2026Article
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
HKDC1 (hexokinase domain containing 1) is recognized as an oncogene in various cancers, yet its role in colorectal cancer (CRC) remains unclear. This study aims to explore HKDC1 expression in CRC and its effects on tumor growth, migration, glycolysis, and EMT, as well as the underlying molecular mechanisms. Using TIMER2.0 and TCGA databases, we analyzed HKDC1 expression across multiple cancers and evaluated its prognostic value via Kaplan-Meier survival analysis. HKDC1 expression in CRC tissues was validated through western blotting, immunohistochemistry, and qRT-PCR, and its correlation with patient prognosis was assessed. Functional experiments involving HKDC1 knockdown and overexpression were performed to examine their impact on CRC cell proliferation, migration, apoptosis, and the cell cycle. Coimmunoprecipitation, immunofluorescence, and mass spectrometry identified HKDC1's interaction with RCOR1, demonstrating its regulation of the Wnt/β-catenin pathway to promote CRC progression. High HKDC1 expression in CRC tissues correlated with poor patient prognosis. Knockdown of HKDC1 significantly reduced cell proliferation and migration, induced G1 phase arrest, and promoted apoptosis, whereas HKDC1 overexpression had the opposite effects. Additionally, HKDC1 promoted EMT and glycolysis through the Wnt/β-catenin signaling pathway. In vivo, HKDC1 knockdown inhibited tumor growth, while overexpression accelerated tumor progression. This study is the first to demonstrate that HKDC1 enhances CRC proliferation, migration, glycolysis, and EMT by modulating RCOR1 and activating the Wnt/β-catenin pathway. These findings suggest that HKDC1 could serve as a potential therapeutic target and prognostic marker for CRC, offering new insights for personalized treatment strategies.
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Registered trials
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