PX-12 modulates vorinostat-induced acetylation and methylation marks in CAL 27 cells.

ABSTRACT:

Aim

The hypoxic tumor microenvironment (TME) in oral squamous cell carcinoma (OSCC) is primarily regulated by hypoxia-inducible factor-1 alpha (HIF-1α), impacting histone acetylation and methylation, which contribute to drug resistance. Vorinostat, a histone deacetylase inhibitor (HDACi), de-stabilizes HIF-1α, while PX-12, a thioredoxin-1 (Trx-1) inhibitor, prevents HIF-1α accumulation. Combining HDACi with a Trx-1 inhibitor may enhance efficacy and reduce resistance by increasing reactive oxygen species (ROS) in cancer cells. This study examines how PX-12 influences vorinostat-induced histone modifications under hypoxia in the OSCC cell line CAL 27 using mass spectrometry.

Materials and methods

The OSCC cell line CAL 27 was used to assess histone post-translational modifica

SUBMITTER: Akhlaq R 

PROVIDER: S-EPMC11792842 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature