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Tumor Microenvironment As a Therapeutic Target in Melanoma Treatment

Overview
Journal Cancers (Basel)
Publisher MDPI
Specialty Oncology
Date 2023 Jun 28
PMID 37370757
Authors
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Abstract

The role of the tumor microenvironment in tumor growth and therapy has recently attracted more attention in research and drug development. The ability of the microenvironment to trigger tumor maintenance, progression, and resistance is the main cause for treatment failure and tumor relapse. Accumulated evidence indicates that the maintenance and progression of tumor cells is determined by components of the microenvironment, which include stromal cells (endothelial cells, fibroblasts, mesenchymal stem cells, and immune cells), extracellular matrix (ECM), and soluble molecules (chemokines, cytokines, growth factors, and extracellular vesicles). As a solid tumor, melanoma is not only a tumor mass of monolithic tumor cells, but it also contains supporting stroma, ECM, and soluble molecules. Melanoma cells are continuously in interaction with the components of the microenvironment. In the present review, we focus on the role of the tumor microenvironment components in the modulation of tumor progression and treatment resistance as well as the impact of the tumor microenvironment as a therapeutic target in melanoma.

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References
1.
Saha S, Lo P, Duan X, Chen H, Wang Q . Breast tumour initiating cell fate is regulated by microenvironmental cues from an extracellular matrix. Integr Biol (Camb). 2012; 4(8):897-904. DOI: 10.1039/c2ib20034a. View

2.
Macleod K, Mullen P, Sewell J, Rabiasz G, Lawrie S, Miller E . Altered ErbB receptor signaling and gene expression in cisplatin-resistant ovarian cancer. Cancer Res. 2005; 65(15):6789-800. DOI: 10.1158/0008-5472.CAN-04-2684. View

3.
Ohtani N . The roles and mechanisms of senescence-associated secretory phenotype (SASP): can it be controlled by senolysis?. Inflamm Regen. 2022; 42(1):11. PMC: 8976373. DOI: 10.1186/s41232-022-00197-8. View

4.
Serban A, Stanca L, Geicu O, Munteanu M, Dinischiotu A . RAGE and TGF-β1 Cross-Talk Regulate Extracellular Matrix Turnover and Cytokine Synthesis in AGEs Exposed Fibroblast Cells. PLoS One. 2016; 11(3):e0152376. PMC: 4807770. DOI: 10.1371/journal.pone.0152376. View

5.
Jin Y, Park I, Hong I, Byun H, Choi J, Kim Y . Fibronectin and vitronectin induce AP-1-mediated matrix metalloproteinase-9 expression through integrin α(5)β(1)/α(v)β(3)-dependent Akt, ERK and JNK signaling pathways in human umbilical vein endothelial cells. Cell Signal. 2010; 23(1):125-34. DOI: 10.1016/j.cellsig.2010.08.012. View