<abstract xmlns="http://www.w3.org/1999/xhtml"><p><bold>Background.</bold> Cancer has traditionally been considered as a disease resulting from gene mutations. New findings in biology are challenging gene-centered explanations of cancer progression and redirecting them to the non-genetic origins of tumorigenicity. It has become clear that intercellular communication plays a crucial role in cancer progression. Among the most intriguing ways of intercellular communication is that via extracellular vesicles (EVs). EVs are membrane structures released from various types of cells. After separation from the mother membrane, EVs become mobile and may travel from the extracellular space to blood and other body fluids.</p><p><bold>Conclusions.</bold> Recently it has been shown that tumour cells are particularly prone to vesiculation and that tumour-derived EVs can carry proteins, lipids and nucleic acids causative of cancer progression. The uptake of tumour-derived EVs by noncancerous cells can change their normal phenotype to cancerous. The suppression of vesiculation could slow down tumour growth and the spread of metastases. The purpose of this review is to highlight examples of EVmediated cancer phenotypic transformation in the light of possible therapeutic applications.</p></abstract>

Background. Cancer has traditionally been considered as a disease resulting from gene mutations. New findings in biology are challenging gene-centered explanations of cancer progression and redirecting them to the non-genetic origins of tumorigenicity. It has become clear that intercellular communication plays a crucial role in cancer progression. Among the most intriguing ways of intercellular communication is that via extracellular vesicles (EVs). EVs are membrane structures released from various types of cells. After separation from the mother membrane, EVs become mobile and may travel from the extracellular space to blood and other body fluids.Conclusions. Recently it has been shown that tumour cells are particularly prone to vesiculation and that tumour-derived EVs can carry proteins, lipids and nucleic acids causative of cancer progression. The uptake of tumour-derived EVs by noncancerous cells can change their normal phenotype to cancerous. The suppression of vesiculation could slow down tumour growth and the spread of metastases. The purpose of this review is to highlight examples of EVmediated cancer phenotypic transformation in the light of possible therapeutic applications.

The role of extracellular vesicles in phenotypic cancer transformation

Laboratory of Biophysics, Faculty of Electrical Engineering, University of Ljubljana, Slovenia

Faculty of Health Sciences, University of Ljubljana, Slovenia

Institute of Cell Biology, Faculty of Medicine, University of Ljubljana, Ljubljana 2, Slovenia

Radiology and Oncology

{"article-title":"The role of extracellular vesicles in phenotypic cancer transformation"}

Background. Cancer has traditionally been considered as a disease resulting from gene mutations. New findings in biology are challenging gene-centered...

The role of extracellular vesicles in phenotypic cancer transformation

Publié en ligne: 30 juil. 2013

Pages: 197 - 205

DOI: https://doi.org/10.2478/raon-2013-0037

This content is open access.