This review summarizes EMT's role in immune evasion in metastatic cancer, suggesting potential therapeutic strategies.
The global prevalence of cancer and its consequential mortality underscores the urgency of understanding the metastatic process, a primary cause of cancer-related deaths. Metastasis, characterized by the spread of cancer cells to distant sites, often involves immune evasion mechanisms facilitating uncontrolled growth. Epithelial-mesenchymal transition (EMT) is a pivotal process enabling metastatic cells to detach from the primary tumor and migrate. EMT induces alterations in surface molecule expression, impairing immune cell recognition. This transition also affects the tumor microenvironment, leading to immune-suppressive cytokine release. The need to investigate EMT-mediated immune evasion is immediate, as it is crucial for developing novel strategies to combat metastatic cancer by targeting these evasive mechanisms. This review aims to summarize molecular changes during EMT, evaluate its impact on surface molecules and the tumor microenvironment that helps it escape from the immune system, and offer insights for devising strategies to target EMT-driven metastatic cells.
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YIGIT KAAN KIZLIER (2024) studied this question.
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