CAFs-released exosomal CREB1 promotes cell progression and immune evasion in thyroid cancer via the positive regulation of CCL20
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View abstract on PubMed
Summary
This summary is machine-generated.Cancer-associated fibroblast exosomes carrying CREB1 promote thyroid cancer progression and immune evasion by upregulating CCL20. Downregulating exosomal CREB1 inhibits tumor growth and enhances T cell function.
Area Of Science
- Oncology
- Cell Biology
- Immunology
Background
- Thyroid cancer (TC) progression is influenced by exosomes from cancer-associated fibroblasts (CAFs).
- CREB1 (cAMP response element binding protein 1) is a transcription factor involved in cancer development.
- The role of exosomal CREB1 and CCL20 in TC remains unclear.
Purpose Of The Study
- To investigate the molecular mechanism of exosome-associated CREB1 and CCL20 in thyroid cancer.
- To elucidate how CAFs-derived exosomes influence the tumor microenvironment in TC.
Main Methods
- RT-qPCR and western blot for gene and protein expression analysis.
- ChIP and dual-luciferase assays for gene interaction.
- Cell migration, invasion, proliferation, and apoptosis assays (wound healing, Transwell, EdU, flow cytometry).
- Exosome characterization and *in vivo* xenograft models.
Main Results
- CREB1 was highly expressed in TC and positively interacted with CCL20, promoting cell migration, invasion, and proliferation.
- CAFs-derived exosomes carrying CREB1 upregulated CCL20, enhancing malignant behaviors and immune evasion.
- Exosomal CREB1 knockdown inhibited tumor progression and improved CD8+ T cell function.
Conclusions
- CAFs-derived exosomes promote thyroid cancer malignancy and immune evasion by delivering CREB1, which upregulates CCL20.
- Targeting exosomal CREB1 offers a potential therapeutic strategy for thyroid cancer.
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