PRMT1 drives oral squamous cell carcinoma progression by activating STAT3 and suppressing ferroptosis via GPX4.

ABSTRACT:

Background

Oral squamous cell carcinoma (OSCC) exhibits poor prognosis due to aggression, metastasis, and chemoresistance. Protein Arginine Methyltransferase 1 (PRMT1) and Signal Transducer and Activator of Transcription 3 (STAT3) are implicated in oncogenesis, but their interplay and downstream effects, particularly concerning ferroptosis and immune evasion in OSCC remain unclear.

Results

PRMT1 was significantly upregulated in OSCC tissues and cell lines, correlating with advanced grade, metastasis, and poor patient survival. PRMT1 knockdown inhibited OSCC proliferation, invasion, metastasis, and chemoresistance in vitro and in vivo. Mechanistically, PRMT1 directly interacted with, methylated, and activated STAT3 (increased p-STAT3 and target genes VEGFA, IL-6, c-myc). The

SUBMITTER: Liu H 

PROVIDER: S-EPMC12642039 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature