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Cell division cycle-associated protein 7 (CDCA7) is a nuclear protein that functions as a transcriptional regulator and plays critical roles in cell cycle progression, chromatin remodeling, and maintenance of DNA methylation patterns. CDCA7 contains a unique zinc-finger domain (zf-4CXXC_R1) that enables it to recognize hemimethylated CpG sites, particularly in non-B-form DNA, and facilitate interactions important for epigenetic regulation. It is a c-Myc-responsive gene involved in oncogenic transformation, and its overexpression is associated with various cancers, where it contributes to tumor cell proliferation, invasion, and resistance to chemotherapeutic drugs such as gemcitabine. In normal physiology, it regulates S-phase progression and heterochromatin maintenance, while inherited mutations in CDCA7 cause immunodeficiency, centromeric instability and facial anomalies (ICF) syndrome. CDCA7 interacts with the transcription factor STAT3, enhancing its activity and promoting glycolytic enzyme transcription, thereby supporting the metabolic needs of rapidly proliferating tumor cells and contributing to drug resistance. Elevated CDCA7 expression is a negative prognostic biomarker in several cancer types.
Modulation of glycolysis via CDCA7-STAT3 axis (regulates hexokinase 2 transcription and cancer cell metabolism); Potential modulation of DNA methylation and chromatin state via interaction with methylated DNA and chromatin remodeling factors
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