REV1‑targeting inhibitor JH‑RE‑06 induces ferroptosis via NCOA4‑mediated ferritinophagy in colorectal cancer cells.

ABSTRACT: Oncogenes accelerate DNA replication, leading to the activation of excessive replication origins. This process triggers replication stress (RS) and genomic instability in cancer cells, positioning RS as a promising therapeutic target. Translesion synthesis (TLS) functions as a DNA damage repair bypass mechanism, compensating for RS and conferring a proliferation advantage to cancer cells. Despite its therapeutic potential, the application of the TLS polymerase REV1 (REV1 DNA directed polymerase (REV1) inhibitor JH‑RE‑06 in colorectal cancer (CRC) remains unexplored. Bioinformatics analysis of clinical samples from The Cancer Genome Atlas (TCGA) database demonstrated marked REV1 upregulation in colorectal tumors compared with normal tissues, which was associated with a poorer prognosis. JH‑

SUBMITTER: Cheng J 

PROVIDER: S-EPMC12485597 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature