# Expression of PD-L1 and p-RPS6 in epithelial dysplasia and squamous cell carcinoma of the oral cavity

## TL;DR

This study examines the expression of PD-L1 and p-RPS6 in oral epithelial dysplasia and squamous cell carcinoma, finding their roles in tumor progression and potential links to the mTOR pathway.

## Contribution

The study reveals a significant positive correlation between PD-L1 and p-RPS6 in oral cancer progression, suggesting a link to the mTOR pathway.

## Key findings

- p-RPS6 was expressed in all cases of OSCC and OED, while PD-L1 was expressed in 87% of OED and 53% of OSCC.
- PD-L1 and p-RPS6 showed a significant positive correlation in both OED and OSCC patients.
- PD-L1 expression was significantly associated with tumor size greater than 2 cm in OSCC patients.

## Abstract

Oral squamous cell carcinoma (OSCC) is often preceded by oral epithelial dysplasia (OED). The role of ribosomal protein S6 (RPS6) and programmed cell death ligand-1 (PD-L1) in the progression of OED to OSCC remains unclear. This study aimed to investigate the expression of phosphorylated RPS6 (p-RPS6) and PD-L1 in OSCC and OED and to examine its relationship with clinicopathological features.

Fifty-two OSCC and 48 OED cases were recruited for immunohistochemical analysis of p-RPS6 and PD-L1 expression. The expression of markers was correlated with clinicopathological features of OSCC and OED.

We found p-RPS6 expression in all cases of OSCC and OED, whereas PD-L1 was expressed in 42/48 (87%) OED and in 28/52 (53%) OSCC. The patients with mild OED presented higher expression level of PD-L1 and p-RPS6 significantly, when compared to moderate-differentiated OSCC patients (p < 0.05). Moreover, we found a significant positive correlation between PD-L1 and p-RPS6 expression in OED and OSCC patients (p < 0.01). The PD-L1 expression was significantly related to more than 2 cm tumor size in OSCC patients (p = 0.007).

Our findings suggest the upregulation of PD-L1 may be related with activation of the mTOR pathway in the early events of tumor progression and the pathogenesis of OSCC.