Scholarship 24/09538-8 - Neoplasias mamárias, Metástase - BV FAPESP
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Exploring the Potential of miRNA-34a as a Regulator of Tumor Growth and Migration: In Vitro Investigation

Grant number: 24/09538-8
Support Opportunities:Scholarships in Brazil - Scientific Initiation
Start date: November 01, 2024
End date: October 31, 2025
Field of knowledge:Health Sciences - Medicine
Principal Investigator:Debora Aparecida Pires de Campos Zuccari
Grantee:Vivian Ayumi Tamane
Host Institution: Faculdade de Medicina de São José do Rio Preto (FAMERP). Secretaria de Desenvolvimento Econômico (São Paulo - Estado). São José do Rio Preto , SP, Brazil

Abstract

Breast cancer is a complex disease involving the uncontrolled proliferation of cells in breast tissue and metastasis. This disease represents the second most common neoplasm in women and has one of the highest mortality rates. The high mortality rates demonstrate the need for a better understanding of the molecular mechanisms involved in metastasis, gene expression control, and the search for alternative therapies. Extracellular vesicles (EVs) are particles enclosed by a lipid bilayer responsible for transporting a variety of molecules, including miRNAs, and are fundamental as mediators of intercellular communication and modulation of the tumor microenvironment. miRNAs are small RNA molecules that play various vital roles in gene expression regulation, acting mainly as tumor suppressors. miRNA-34a stands out as one of the main miRNAs with tumor suppressor potential. Recognized for its ability to inhibit tumor cell proliferation and modulate various signaling pathways, this miRNA is essential for controlling tumor growth. In many breast cancer diagnoses, a significant reduction in miRNA-34a expression is observed, which further compromises the control of cell proliferation. Extracellular vesicles (EVs) loaded with miRNA-34a can be transferred between cells, directly impacting the gene expression and cellular functions of recipient cells. This phenomenon has the potential to modulate the regulation of the PI3K/Akt/mTOR pathway and other cancer-related processes. In this context, loading EVs with miRNA-34a emerges as a promising approach in carcinoma treatment, especially in cases characterized by excessive activation of the PI3K/Akt/mTOR pathway. Therefore, this study aims to propose an intervention to mitigate the growth and metastasis of breast cancer through EV/miRNA-34a therapy.

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