? Extracellular vesicles in breast cancer Microenvironment: the mechanisms underlying endocrine resistance

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Congreso; reunion conjunta sai saic nanomedicina; 2021

(373) EXTRACELLULAR VESICLES IN BREAST CANCERMICROENVIRONMENT: THE MECHANISMS UNDERLYINGENDOCRINE RESISTANCERodriguez-Baili MC, Gil GACIQUIBIC-CONICET. Quimica Biologica Ranwel Caputto,FCQ.UNC. CP:5000Antiestrogen adjuvant treatments are first-line therapies in patientswith estrogen receptor-positive (ER +) breast cancer. The treatmentstrategies need to be improved because most patients eventuallybecome endocrine resistant and many others are initially refractoryto anti-estrogen treatments. The tumor microenvironment, andmainly macrophages, play an essential role in the development andprogress of cancer; however, the molecular mechanisms underlyingthese effects remain poorly understood. Extracellular vesicles (EVs)secreted by tumor cells or by cells from the microenvironment havebeen proposed as one of the main forms of cell-cell communication.Many reports involve them in processes that are essential for cancerprogression such as proliferation, migration, endocrine resistance,invasion, administration of drugs, among others. We proposed thatEV are one of the most important actors in cell communication andcould be one of the responsible for the endocrine resistance thatwe had observed in our previous work. The first steps for the studyof these vesicles are the isolation and characterization of EVs fromour cells of interest, then we evaluate the effect of EVs from macrophagesand activated macrophages on mammary cells (tumorand non-tumor). These results suggest that EVs are involved in increasedproliferation of mammary cells, and this increase dependson the amount and type of EVs, as well as the recipient cells. Thisand other analyzes will allow us to determine whether EVs are involvedin communication between tumor-associated macrophages(TAMs) and tumor cells, and whether they are responsible for endocrineresistance in estrogen receptor-positive breast cancers.