Gallic acid chemoprevention of oral carcinogenesis

Naturally derived phytochemicals such as gallic acid (GA) exhibit multitargeted anticancer properties and favorable safety profiles, yet the molecular mechanisms underlying their chemopreventive effects in head and neck squamous cell carcinoma (HNSCC) remain incompletely defined. Using a 4 nitroquinoline 1 oxide (4NQO) induced oral carcinogenesis mouse model, we evaluated GA’s effects on tumor progression, and related molecular pathways. Phenotypic outcomes were assessed by histopathology, and proliferation markers. Transcriptomic changes were profiled by RNA sequencing, pathway enrichment and validation using RT qPCR. We report GA as a key modulator of transcriptional programs associated with oral carcinogenesis in a 4-nitroquinoline-1-oxide–induced mouse model. Comparative RNA sequencing of wild-type vehicle-treated (WtVeh) and GA-treated (WtGal) oral tissues revealed GA-dependent reprogramming of immune and stress-response pathways. Our data identifies unique molecular pathways associated with GA mediated oral cancer chemoprevention.