PPARγ accelerates OSCC progression via Th17 polarization and CEBPA/IL-17C signaling.

ABSTRACT:

Background

Oral squamous cell carcinoma (OSCC) is a marked invasive epithelial tumor with limited treatment efficacy, especially in advanced stages. The immunosuppressive nature of the tumor microenvironment (TME) is a major contributor to OSCC development and therapeutic resistance. Peroxisome proliferator-activated receptor gamma (PPARγ) is known to influence tumor biology in a multifaceted and context-specific manner. The objective of this research was to explore the role of PPARγ in modulating the TME and its impact on OSCC progression.

Methods

A 4NQO-induced OSCC model was used to verify PPARγ overexpression by Immunohistochemistry (IHC). Bulk RNA-seq and single-cell RNA-seq analyses were employed to dissect PPARγ-driven tumor-promoting mechanisms. Co-cultivation of OSC

SUBMITTER: Wang Y 

PROVIDER: S-EPMC12436265 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature