Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2019 Jun 19;9:521. doi: 10.3389/fonc.2019.00521

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2019 Mannavola, Salerno, Passarelli, Tucci, Internò and Silvestris.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

PMC Copyright notice

Mechanisms responsible for Exosome-mediated drug resistance in CRC. Exosomes released by either tumor cells (Tumor-derived Exos) or cancer associated fibroblasts (CAF-derived Exos) cooperate to induce resistance of CRC against targeted and cytotoxic drugs. This process is mediated by exosomal delivery of non-coding RNAs into cancer cells leading to the stimulation of mTOR and STAT3 intracellular signaling, as well as to the acquisition of cancer stemness features. Additionally, sequestration of anti-EGFR (panitumumab and cetuximab) and anti-VEGF (bevacizumab) monoclonal antibodies (MoAbs) by Tumor-derived Exos is another possible mechanism reducing the bioavailability of these drugs and defective anti-cancer activity.