AI Article Synopsis

  • * Key interactions involve changes in cell behavior like epithelial-mesenchymal transformation, disruptions in iron metabolism in cancer stem cells, macrophage polarization, and the impact of iron levels on immune responses and blood vessel formation.
  • * The review emphasizes how microRNAs related to ferroptosis can influence tumor metastasis by affecting cancer and immune cell interactions, cytokine regulation, and angiogenesis, presenting new avenues for potential cancer treatments.

Article Abstract

Ferroptosis, a novel mode of cell death dependent on iron and reactive oxygen species, has been extensively explored during malignant tumors metastasis. Ferroptosis can interact with multiple components of the tumor microenvironment to regulate metastasis. These interactions generally include the following aspects: (1) Epithelial-mesenchymal transformation, which can help cancer cells increase their sensitivity to ferroptosis while they have multiple mechanisms to fight against it; (2) Disorder of iron metabolism in cancer stem cells which maintains their stem characteristics; (3) Polarization of M0 macrophages to M2. (4) The paradoxical effects of iron metabolism and CD8 + T cells induced by ferroptosis (5) Regulation of angiogenesis. In addition, ferroptosis can be regulated by miRNAs through the reprogramming of various intracellular metabolism processes, including the regulation of the glutathione- glutathione peroxidase 4 pathway, glutamic acid/cystine transport, iron metabolism, lipid metabolism, and oxidative stress. Therefore, there are many potential interactions between ferroptosis-related miRNAs and tumor metastasis, including interaction with cancer cells and immune cells, regulating cytokines, and angiogenesis. This review focuses on the role of ferroptosis-related miRNA in tumor metastasis, aiming to help readers understand their relationship and provide a new perspective on the potential treatment strategies of malignant tumors.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10300116PMC
http://dx.doi.org/10.1038/s41420-023-01486-yDOI Listing

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