Extracellular Vesicles Shedding Promotes Melanoma Growth in Response to Chemotherapy.

Extracellular Vesicles Shedding Promotes Melanoma Growth in Response to Chemotherapy.

Publication date: Oct 09, 2019

Extracellular vesicles (EVs) are emerging as key players in intercellular communication. EVs can transfer biological macromolecules to recipient cells, modulating various physiological and pathological processes. It has been shown that tumor cells secrete large amounts of EVs that can be taken up by malignant and stromal cells, dictating tumor progression. In this study, we investigated whether EVs secreted by melanoma cells in response to chemotherapy modulate tumor response to alkylating drugs. Our findings showed that human and murine melanoma cells secrete more EVs after treatment with temozolomide and cisplatin. We observed that EVs shed by melanoma cells after temozolomide treatment modify macrophage phenotype by skewing macrophage activation towards the M2 phenotype through upregulation of M2-marker genes. Moreover, these EVs were able to favor melanoma re-growth in vivo, which was accompanied by an increase in Arginase 1 and IL10 gene expression levels by stromal cells and an increase in genes related to DNA repair, cell survival and stemness in tumor cells. Taken together, this study suggests that EVs shed by tumor cells in response to chemotherapy promote tumor repopulation and treatment failure through cellular reprogramming in melanoma cells.

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Andrade, L.N.S., Otake, A.H., Cardim, S.G.B., da Silva, F.I., Ikoma Sakamoto, M.M., Furuya, T.K., Uno, M., Pasini, F.S., and Chammas, R. Extracellular Vesicles Shedding Promotes Melanoma Growth in Response to Chemotherapy. 24419. 2019 Sci Rep (9):1.

Concepts Keywords
Chemotherapy Murine melanoma
Cisplatin Chemotherapy
IL10 Branches of biology
Intercellular Communication Medicine
Macromolecules Clinical medicine
Macrophage Cancer treatments
Malignant Vesicles
Melanoma Oncology
Murine Cell biology
Phenotype Extracellular vesicle
Sci Melanoma
Stemness Temozolomide
Stromal Chemotherapy
Temozolomide Chemotherapy
Tumor
Vesicles
Vivo

Semantics

Type Source Name
gene UNIPROT MRC1
gene UNIPROT SLC26A5
gene UNIPROT RERE
gene UNIPROT ABL2
drug DRUGBANK L-Arginine
drug DRUGBANK Dimethyl sulfoxide
gene UNIPROT FBXO8
gene UNIPROT FBRS
gene UNIPROT CD63
gene UNIPROT CD9
gene UNIPROT RNF2
gene UNIPROT DEPP1
gene UNIPROT GOPC
gene UNIPROT NDE1
gene UNIPROT TALDO1
gene UNIPROT LRSAM1
disease DOID gastric cancer
disease MESH gastric cancer
pathway BSID Immune System
gene UNIPROT FN1
pathway BSID Pancreatic cancer
disease DOID pancreatic cancer
disease MESH pancreatic cancer
disease DOID gastric carcinoma
gene UNIPROT MLXIP
gene UNIPROT MYLIP
gene UNIPROT MARCH8
disease MESH hypoxia
pathway BSID Angiogenesis
drug DRUGBANK Docetaxel
disease DOID prostate cancer
pathway BSID Prostate cancer
disease MESH prostate cancer
disease DOID GBM
gene UNIPROT MET
gene UNIPROT SLTM
drug DRUGBANK Methionine
gene UNIPROT PTPRZ1
disease MESH glioblastoma
disease DOID breast tumor
disease MESH breast tumor
drug DRUGBANK Paclitaxel
disease DOID adenocarcinoma
disease MESH adenocarcinoma
disease MESH gliomas
gene UNIPROT EHD1
pathway BSID Budding
disease MESH multi
drug DRUGBANK Coenzyme M
disease MESH treatment failure
pathway BSID DNA Repair
pathway BSID Gene Expression
gene UNIPROT IL10
drug DRUGBANK Cisplatin
drug DRUGBANK Temozolomide
gene UNIPROT LARGE1
disease MESH tumor
disease MESH pathological processes
disease MESH Growth
pathway BSID Melanoma
disease DOID Melanoma
disease MESH Melanoma

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