Transcription factor SP1 drives the malignant progression of oral squamous cell carcinoma and M2 macrophage polarization through transcription activation-mediated upregulation CLEC7A
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View abstract on PubMed
Summary
This summary is machine-generated.C-Type Lectin Domain Containing 7A (CLEC7A) drives oral cancer progression by promoting M2 macrophage polarization. Targeting the SP1-CLEC7A pathway could offer new treatments for oral squamous cell carcinoma (OSCC).
Area Of Science
- Oncology
- Immunology
- Molecular Biology
Background
- Oral squamous cell carcinoma (OSCC) is a prevalent oral malignancy.
- C-Type Lectin Domain Containing 7A (CLEC7A) is implicated in cancer progression via M2 macrophage polarization.
- The precise molecular mechanisms of CLEC7A in OSCC remain unclear.
Purpose Of The Study
- To elucidate the molecular mechanism of CLEC7A in OSCC progression.
- To investigate the role of SP1 in regulating CLEC7A expression and function in OSCC.
- To explore the therapeutic potential of targeting the SP1-CLEC7A axis in OSCC.
Main Methods
- Bioinformatic analysis (GEPIA database) of CLEC7A and SP1 expression.
- Gene expression analysis (RT-qPCR) and protein level detection (Western blot).
- Functional assays for cell proliferation, apoptosis, migration, and invasion (Colony formation, flow cytometry, Transwell assays).
- Macrophage polarization assessment (flow cytometry).
- Molecular mechanism validation (JASPAR, ChIP, dual-luciferase reporter assays).
- In vivo tumor growth assessment (xenograft model).
Main Results
- CLEC7A and SP1 expression are upregulated in OSCC tissues and cell lines.
- CLEC7A deficiency inhibits OSCC cell proliferation, migration, invasion, M2 polarization, and tumor growth, while promoting apoptosis.
- SP1 acts as a transcription factor for CLEC7A, binding to its promoter and enhancing transcription.
- SP1-induced CLEC7A facilitates OSCC malignancy and M2 macrophage polarization.
Conclusions
- SP1-mediated upregulation of CLEC7A is a key driver of OSCC progression.
- The SP1-CLEC7A pathway significantly influences OSCC cell behaviors and the tumor microenvironment.
- Targeting the SP1-CLEC7A axis presents a promising therapeutic strategy for OSCC.
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