Title:PPT1 Promotes Growth and Inhibits Ferroptosis of Oral Squamous Cell
Carcinoma Cells
Volume: 24
Issue: 10
Author(s): Qingqiong Luo, Sheng Hu, Yijie Tang, Dandan Yang and Qilong Chen*
Affiliation:
- Department of Clinical Immunology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of
Medicine, 200011, Shanghai, China
- Central Laboratory, Shanghai Skin Disease Hospital, School
of Medicine, Tongji University, Shanghai, 200443, China
Keywords:
Oral squamous cell carcinoma, differentially expressed genes, palmitoyl-protein thioesterase 1, proliferation, glutathione peroxidase 4, ferroptosis.
Abstract:
Background: Oral squamous cell carcinoma (OSCC) is one of the most prevalent cancers
with poor prognosis in the head and neck. Elucidating molecular mechanisms underlying
OSCC occurrence and development is important for the therapy. Dysregulated palmitoylation-related
enzymes have been reported in several cancers but OSCC.
Objectives: To explore the role of palmitoyl-protein thioesterase 1 (PPT1) in OSCC.
Methods: Differentially expressed genes (DEGs) and related protein-protein interaction networks
between normal oral epithelial and OSCC tissues were screened and constructed
via different online
databases. Tumor samples from 70 OSCC patients were evaluated for the relationship between
PPT1 expression level and patients’clinic characteristics. The role of PPT1 in OSCC proliferation
and metastasis was studied by functional experiments including MTT, colony formation,
EdU incorporation and transwell assays. Lentivirus-based constructs were used to manipulate
gene expression. FerroOrange probe and malondialdehyde assay were used to determine ferroptosis.
Growth of OSCC cells
in vivo was investigated by a xenograft mouse model.
Results: A total of 555 DEGs were obtained, and topological analysis revealed that PPT1 and
GPX4 might play critical roles in OSCC. Increased PPT1 expression was found to be correlated
with poor prognosis of OSCC patients. PPT1 effectively promoted the proliferation, migration and
invasion while inhibited the ferroptosis of OSCC cells. PPT1 affected the expression of glutathione
peroxidase 4 (GPX4).
Conclusion: PPT1 promoted growth and inhibited ferroptosis of OSCC cells. PPT1 might be a potential
target for OSCC therapy.
