ArticleCellular & molecular biology letters2026
PRKN mediates the ubiquitination of SCAF8 to reduce the mRNA stability of KLF5 and its transcriptional activation of EFNA3 in colorectal cancer.
Article in Cellular & molecular biology letters, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundDysregulation in glycolysis within the tumor microenvironment is a hallmark in the context of colorectal cancer (CRC). We aimed to identify critical drivers of glycolysis in CRC and decipher the underlying mechanism.
methodsThrough combined gene interference in CRC cells using lentivirus and treatment with glycolysis activator DASA-58, we measured glycolytic flux to evaluate how molecular mechanisms influence tumor cell activity via glycolysis. CRC cells were cocultured with NK and CD8
resultsEFNA3 was elevated in CRC tissues and cell lines. The glycolytic activity, proliferative, migratory, invasive, and pro-angiogenic effects of the CRC cells were reduced, and the anti-tumor response of the CD
conclusionsActivating the E3 ubiquitin ligase activity of PRKN to suppress EFNA3 expression represents a promising therapeutic strategy for the clinical treatment of CRC.
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