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Updated: Aug 14, 2026
Isolation and Characterization of a Head and Neck Squamous Cell Carcinoma Subpopulation Having Stem Cell Characteristics
Published on: May 11, 2016
TRIM32 drives head and neck squamous cell carcinoma progression via TP53 suppression and lysosomal/autophagy
Langxiong Chen1,2, Yuyang Zhang1,2, Huaying Liao1,2
1Guangzhou Institute of Cancer Research, the Affiliated Cancer Hospital, Guangzhou Medical University, Guangzhou, China.
Background:
The TRIM32 has been implicated in tumorigenesis across various cancers; however, its functional significance in head and neck squamous cell carcinoma (HNSCC) requires systematic investigation. This study sought to explore the expression and biological function of TRIM32 in HNSCC tissues to identify new targets or biomarkers for HNSCC diagnosis and treatment.
Methods:
HNSCC samples were extracted for TRIM32 expression profiling, with subsequent integration of clinical samples for validation. Gene Set Enrichment Analysis (GSEA) was performed using the c2.cp.kegg.v7.4.symbols.gmt gene set. Immune cell infiltration was evaluated using the ESTIMATE algorithm. Following TRIM32 knockdown via small interfering RNA (siRNA) in HNSCC cell lines (HSC-3, FADU), proliferation and invasion capacities were assessed using Cell Counting Kit-8 (CCK-8) and Transwell assays, respectively. Western blotting was conducted to analyse protein expression within the TRIM32-p53-LAMP1/2-LC3B pathway.
Results:
Integrated bioinformatics analysis and clinical sample validation revealed significantly elevated TRIM32 expression in HNSCC, correlating with poor patient prognosis. GSEA demonstrated significant enrichment of autophagy and p53 signalling pathways within the TRIM32 high-expression group. In vitro experiments confirmed that TRIM32 silencing suppressed proliferation and invasion capacities in HSC-3 and FADU cell lines. Western blotting further delineated that TRIM32 regulates autophagic flux through the TRIM32-p53-LAMP1/2-LC3B axis. The ESTIMATE algorithm indicated a significant association between TRIM32 expression and immune cell infiltration, suggesting a potential role in remodelling the tumour immune microenvironment.
Conclusions:
TRIM32 expression is significantly elevated in HNSCC, indicating its potential as an adverse prognostic marker. Experimental evidence demonstrates that TRIM32 facilitates cellular proliferation and migration, significantly influences lysosomal function and autophagy processes within HNSCC cells, and is verified to negatively regulate tumour protein 53 (TP53). These mechanisms contribute to the aggressive behaviour of HNSCC.
Insights
Tripartite motif 32 (TRIM32) is elevated in head and neck squamous cell carcinoma (HNSCC), promoting cancer cell proliferation and migration. TRIM32 influences autophagy and negatively regulates TP53, contributing to HNSCC
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Tripartite motif 32 (TRIM32) is implicated in various cancers.
- Its specific role in head and neck squamous cell carcinoma (HNSCC) requires detailed investigation.
Purpose of the Study:
- To investigate TRIM32 expression and function in HNSCC.
- To identify TRIM32 as a potential diagnostic or therapeutic target for HNSCC.
Main Methods:
- TRIM32 expression profiling in HNSCC tissues and clinical samples.
- Gene Set Enrichment Analysis (GSEA) and ESTIMATE algorithm for immune cell infiltration.
- In vitro studies using TRIM32 knockdown in HNSCC cell lines (HSC-3, FADU) to assess proliferation and invasion.
- Western blotting to analyze the TRIM32-p53-LAMP1/2-LC3B pathway.
Main Results:
- Elevated TRIM32 expression in HNSCC correlates with poor prognosis.
- TRIM32 high-expression is linked to enriched autophagy and p53 signaling pathways.
- TRIM32 silencing reduced HNSCC cell proliferation and invasion.
- TRIM32 regulates autophagic flux via the TRIM32-p53-LAMP1/2-LC3B axis and impacts immune cell infiltration.
Conclusions:
- TRIM32 is a potential adverse prognostic marker in HNSCC.
- TRIM32 promotes HNSCC aggressiveness by facilitating proliferation, migration, and influencing autophagy and p53.
- TRIM32 may play a role in modulating the tumor immune microenvironment.
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