Title:Proteomic Analysis of the Molecular Mechanisms of Chlorpromazine
Inhibiting Migration of Oral Squamous Cell Carcinoma
Volume: 21
Issue: 1
Author(s): Nannan Zhang, Junzhi Liu, Qiuping Dong, Chen Liu, Xinyu Liang, Peiyuan Tang and Zheng Liang*
Affiliation:
- Department of Otorhinolaryngology, Tianjin Medical University General Hospital, Tianjin, 300020, China
Keywords:
Chlorpromazine, oral squamous cell carcinoma, proteomics, liquid chromatography-mass spectrometry, cell migration, molecular docking.
Abstract:
Background: Oral squamous cell carcinoma (OSCC) is a common malignant tumor of
the head and neck region known for its high metastatic and invasive potential. Chlorpromazine
(CPZ) has been shown to inhibit the growth of oral cancer cells. However, the effects of CPZ on
OSCC migration and its underlying molecular mechanisms remain unclear.
Objectives: We aimed to identify global protein changes and potential core proteins involved in
CPZ-mediated inhibition of migration in SCC-15 cells using proteomics.
Methods: We assessed the effect of CPZ on SCC-15 using CCK-8 assays and wound healing experiments.
Next, we performed LC-MS-based proteomic analysis to identify protein alterations in
SCC-15 cells treated with CPZ at different times. Differential expression proteins (DEPs) were
identified and subjected to bioinformatics analysis using GO, KEGG, and PPI tools. Key candidate
proteins were selected and validated using the TCGA-HNSCC database and molecular docking.
Results: It was found that 20μm of CPZ had no effect on cell proliferation, but inhibited cell migration.
A total of 4748 proteins were identified by Proteomics, among which 56 DEPs were identified,
including 34 upregulated proteins and 22 downregulated proteins. Three proteins (RPF2,
ACTB, and TGFBI) were identified as key candidate proteins associated with cell adhesion and
migration in oral cancer cells.
Conclusion: CPZ may affect the expression of RPF2, ACTB, and TGFBI proteins and change the
extracellular matrix and cell adhesion function, thus inhibiting the migration of SCC-15 cells. The
results of this study provide a robust basis for further research on the molecular mechanism of
CPZ to inhibit the migration of OSCC.