Colorectal cancer (CRC) is a heterogeneous disease driven by complex genetic, epigenetic, and microenvironmental alterations. Members of the PR domain-containing (PRDM) protein family have emerged as context-dependent regulators of CRC initiation, progression, tumor cell plasticity, immune modulation, and therapeutic response. Accumulating evidence highlights divergent roles for PRDM proteins as tumor suppressors, oncogenes, or isoform-dependent dual-function regulators. Collectively, PRDM family members represent a central node of transcriptional/epigenetic control in CRC biology, with significant potential as biomarkers for early detection, prognosis, and treatment stratification, as well as promising candidates for epigenetic and pathway-directed therapeutic strategies.

PRDM Proteins Orchestrate Colorectal Cancer Tumorigenesis

Fiore, Donatella
Membro del Collaboration Group
;
Proto, Maria Chiara
Membro del Collaboration Group
;
Gazzerro, Patrizia
Supervision
;
2026

Abstract

Colorectal cancer (CRC) is a heterogeneous disease driven by complex genetic, epigenetic, and microenvironmental alterations. Members of the PR domain-containing (PRDM) protein family have emerged as context-dependent regulators of CRC initiation, progression, tumor cell plasticity, immune modulation, and therapeutic response. Accumulating evidence highlights divergent roles for PRDM proteins as tumor suppressors, oncogenes, or isoform-dependent dual-function regulators. Collectively, PRDM family members represent a central node of transcriptional/epigenetic control in CRC biology, with significant potential as biomarkers for early detection, prognosis, and treatment stratification, as well as promising candidates for epigenetic and pathway-directed therapeutic strategies.
File in questo prodotto:
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11386/4954555
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus 0
  • ???jsp.display-item.citation.isi??? 0
social impact