Abstract

Cancer is one of the leading diseases, causing deaths worldwide. Nearly 10 million deaths were reported in 2020 due to cancer alone. Several factors are involved in cancer progressions, such as lifestyle and genetic characteristics. According to a recent report, extracellular vesicles (EVs) are involved in cancer initiation, progression, and therapy failure. EVs can play a major role in intracellular communication, the maintenance of tissue homeostasis, and pathogenesis in several types of diseases. In a healthy person, EVs carry different cargoes, such as miRNA, lncRNA etc., to help other body functions. On the other hand, the same EV in a tumor microenvironment carries cargoes such as miRNA, lncRNA, etc., to initiate or help cancer progression at various stages. These stages may include the proliferation of cells and escape from apoptosis, angiogenesis, cell invasion, and metastasis, reprogramming energy metabolism, evasion of the immune response, and transfer of mutations. Tumor-derived EVs manipulate by altering normal functions of the body and affect the epigenetics of normal cells by limiting the genetic makeup through transferring mutations, histone modifications, etc. Tumor-derived EVs also pose therapy resistance through transferring drug efflux pumps and posing multiple drug resistances. Such EVs can also help as biomarkers for different cancer types and stages, which ultimately help with cancer diagnosis at early stages. In this review, we will shed light on EVs’ role in performing normal functions of the body and their position in different hallmarks of cancer, in altering the genetics of a normal cell in a tumor microenvironment, and their role in therapy resistance, as well as the importance of EVs as diagnostic tools.

Highlights

  • This article is an open access articleCancer is a disease in which the body’s cells grow uncontrollably and spread throughout

  • It is observed that in breast cancer patients having (Adriamycin) resistance to chemotherapy had higher amounts of Glutathione S-transferase P1 (GSTP1) in comparison to those patients who responded to the therapy, interestingly, through the transfer of miR-122 cargo of extracellular vesicles (EVs) secreted by breast cancer cells, changed glucose metabolism in recipient non-tumor cells, facilitating disease progression [7,78]

  • In the presence of EVs produced by pancreatic cancer cell lines, primary pancreatic fibroblasts from mice were transformed into cancer-associated fibroblasts (CAFs)-like cells, a process controlled by miR155 found in the EVs’ cargo [116]

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Summary

Introduction

Cancer is a disease in which the body’s cells grow uncontrollably and spread throughout. Carcinoma in situ is a clump of abnormal cells that will not migrate beyond the site where they first developed, but they may subsequently spread into normal tissue and cause cancer. The specific functions of EVs depend on the cell source and origin

Cell Source of EVs
B Lymphocytes
Intracellular Transfer of Traits between Microenvironment and Tumor Cells
Derived EVs and Epigenetic Biology of EVs
Methylation of DNA Influenced by EVs
RNAs and EVs as the Key Players for Cancer Progression
Tumor-Derived EVs and Their Approaches in Disease Progression
Initiation
Progression
Metastasis
Therapy Failure
Role of EVs in Aiding Cell to Escape from Apoptosis
Reprogramming Energy Metabolism
Angiogenesis
Evasion of Immune Response
Fibroblasts
T lymphocytes
Macrophages
NK and Dendritic Cells
Transfer of Mutations
Derived EVs and Therapy Resistance
Drug Efflux Pumps and Their Transfer
Anti-Apoptotic Pathways and Their Development
Transfer of Proteins and Lipids
EVs as a Diagnostic Tool
EVs as a Tool for Cancer Therapy
Drug Delivery Vehicle
EVs as Vaccines
EVs in Gene Therapy
Findings
10. Conclusions
Full Text
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