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ENO1 Promotes OSCC Migration and Invasion by Orchestrating IL-6 Secretion from Macrophages via a Positive Feedback
Ying Lin1, Wenwen Zhang1, Luyao Liu1
1Jilin Provincial Key Laboratory of Oral Biomedical Engineering, Department of Oral Anatomy and Physiology, Hospital of Stomatology, Jilin University, Changchun 130021, China.
International Journal of Molecular Sciences
|January 8, 2023
Summary
Alpha-enolase (ENO1) drives oral squamous cell carcinoma (OSCC) progression by promoting tumor cell invasion and metastasis. ENO1 orchestrates macrophage IL-6 secretion, creating a positive feedback loop that enhances OSCC growth and offers a potential therapeutic target.
Area of Science:
- Oncology
- Cell Biology
- Immunology
Background:
- Oral squamous cell carcinoma (OSCC) exhibits high invasion and metastasis rates, leading to poor survival.
- Tumor cell-macrophage interactions are crucial for OSCC progression, but underlying mechanisms remain unclear.
Purpose of the Study:
- To investigate the role of tumor cell-derived alpha-enolase (ENO1) in mediating OSCC cell and macrophage interactions.
- To elucidate the specific molecular pathways involved in ENO1-driven OSCC progression.
Main Methods:
- Utilized small interfering RNA (siRNA) to reduce ENO1 levels and recombinant human ENO1 (rhENO1) for stimulation.
- Analyzed ENO1 expression, lactic acid release, and macrophage conditioned medium (Macro-CM) effects on OSCC cells.
- Investigated the involvement of epithelial-mesenchymal transition (EMT), IL-6, and the ENO1/Toll-like receptor 4 (TLR4) pathway.
Main Results:
- ENO1 expression was elevated in OSCC cells (CAL27) compared to normal cells (HaCaT) and regulated lactic acid release.
- Macrophage conditioned medium (Macro-CM) increased ENO1 mRNA and protein in OSCC cells.
- ENO1 promoted OSCC cell migration and invasion via EMT induction in macrophages and orchestrated macrophage IL-6 secretion through lactic acid and the ENO1/TLR4 pathway.
Conclusions:
- ENO1 promotes OSCC cell migration and invasion by orchestrating macrophage IL-6 secretion via a dual mechanism, establishing a positive feedback loop.
- This ENO1-mediated crosstalk significantly contributes to OSCC progression.
- ENO1 represents a potential therapeutic target for controlling OSCC advancement.
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