Expression of PD-L1 and p-RPS6 in epithelial dysplasia and squamous cell carcinoma of the oral cavity
Issued Date
2024-01-01
Resource Type
eISSN
26734842
Scopus ID
2-s2.0-85185119043
Journal Title
Frontiers in Oral Health
Volume
5
Rights Holder(s)
SCOPUS
Bibliographic Citation
Frontiers in Oral Health Vol.5 (2024)
Suggested Citation
Hanroongsri J., Amornphimoltham P., Younis R.H., Chaisuparat R. Expression of PD-L1 and p-RPS6 in epithelial dysplasia and squamous cell carcinoma of the oral cavity. Frontiers in Oral Health Vol.5 (2024). doi:10.3389/froh.2024.1337582 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/97308
Title
Expression of PD-L1 and p-RPS6 in epithelial dysplasia and squamous cell carcinoma of the oral cavity
Corresponding Author(s)
Other Contributor(s)
Abstract
Introduction: 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. Methods: 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. Results: 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). Discussion: 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.