Abstract
Epithelial–mesenchymal transition (EMT) and metabolic reprogramming in cancer cells are the key hallmarks of tumor metastasis. Since the relationship between the two has been well studied, researchers have gained increasing interest in the interplay of cancer cell EMT and immune metabolic changes. Whether the mutual influences between them could provide novel explanations for immune surveillance during metastasis is worth understanding. Here, we review the role of immunometabolism in the regulatory loop between tumor-infiltrating immune cells and EMT. We also discuss the challenges and perspectives of targeting immunometabolism in cancer treatment.
Highlights
Metastasis is the primary cause of cancer-related mortality, which can occur early through parallel progression along with the primary tumor or late after linear tumor progression [1]
Compared to the extensive understanding of metabolic alterations in cancer cells during metastasis, the role of metabolic reprogramming in tumor-associated immune cells and whether the process has mutual effects with epithelialmesenchymal transition (EMT) are the key questions that have not been investigated in depth
When combined with antiPD-1, the results indicated durable antitumor responses by preventing the presentation of PD-1+/CD8+ T-cell infiltrates after drug withdrawal [187]; we should acknowledge the fact that the recently reported first-generation clinical trials using metformin in combination with systemic therapy have failed to significantly improve outcomes in cancer patients [188,189]
Summary
Metastasis is the primary cause of cancer-related mortality, which can occur early through parallel progression along with the primary tumor or late after linear tumor progression [1]. During an EMT, specific changes are required by the cancer cells to migrate and colonize distant organs, including changes in intrinsic tumor cell properties and the tumor microenvironment (TME), as well as those affecting the crosstalk between the two compartments mentioned above. Amongst these changes, metabolic reprogramming has been suggested as a key hallmark of cancer progression [4,5]. Compared to the extensive understanding of metabolic alterations in cancer cells during metastasis, the role of metabolic reprogramming in tumor-associated immune cells and whether the process has mutual effects with EMT are the key questions that have not been investigated in depth.
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