Newly identified C/EBPγ protein links cancer cell plasticity and DNA repair
A research team has identified the transcription factor C/EBPγ as a novel regulator that simultaneously promotes epithelial-mesenchymal transition (EMT) and DNA double-strand break repair in lung adenocarcinoma cells. The findings, published in Cell Death Discovery, provide new insights into how cancer cells acquire aggressive features and resistance to anticancer treatments.
Researchers have identified a novel transcription factor, C/EBPγ, that plays a dual role in cancer cell behavior. First, C/EBPγ promotes epithelial-mesenchymal transition (EMT), a process that enhances cancer cell mobility, invasiveness, and adaptability, which are associated with tumor progression and resistance to therapy. Second, C/EBPγ enhances DNA repair mechanisms, specifically the non-homologous end joining (NHEJ) pathway, which allows cancer cells to survive DNA-damaging treatments.
This dual function of C/EBPγ provides new insights into how cancer cells acquire aggressive features and resist anticancer therapies.
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