Tumor Immune Microenvironment during Epithelial-Mesenchymal Transition

Area of Science:

• Oncology
• Immunology
• Molecular Biology

Background:

• Epithelial-mesenchymal transition (EMT) is crucial in tumor progression, from initiation to metastasis.
• EMT is a dynamic process, involving hybrid phenotypes with high plasticity.
• EMT is linked to tumor immune evasion, affecting immunosuppressive cells and immune checkpoints.

Purpose of the Study:

• To elucidate the intricate relationship between EMT and tumor immunosuppression.
• To explore the molecular mechanisms driving the feedback loop between EMT and immunosuppression.
• To identify potential therapeutic strategies by targeting the EMT-immunosuppression axis.

Main Methods:

• Review of existing literature on EMT and tumor immunology.
• Analysis of molecular pathways involving EMT transcriptional factors (Snail, Zeb1, Twist1).
• Examination of the role of chemokines and immunosuppressive factors in the tumor microenvironment.

Main Results:

• EMT promotes an immunosuppressive microenvironment by attracting myeloid-derived suppressor cells and upregulating immune checkpoints like PD-L1.
• EMT transcriptional factors mediate immunosuppression through chemokine production.
• A reciprocal feedback loop exists where immunosuppressive factors can induce EMT in tumor cells.

Conclusions:

• The interplay between EMT and immunosuppression significantly drives tumor progression.
• Targeting EMT directly is challenging, necessitating a focus on the EMT-immunosuppression axis.
• Combination therapies involving immune checkpoint inhibitors and agents targeting immunosuppressive cells show promise for EMT-driven cancers.