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. 2022 Mar 25;23(7):3620. doi: 10.3390/ijms23073620

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© 2022 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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The contribution of the PDAC microenvironment to the generation of drug resistance. (A) GEM-treated PDAC cells secrete miR-155 through exosomes enhancing the antioxidant capacity of cancer cells (through the downregulation of SOD2 and CAT), disrupting the activation of GEM (through the downregulation of DCK) and cellular stress-sensing systems (by upregulating TP53INP1). (B) GEM-treated CAFs exosomally secreted miR-106b, miR-146a, and Snail, all of which mediate their intrinsic resistance to GEM. (C) The M2-derived exosomally excreted miR-365 increased the intracellular NTP pool and the CDA. (D) GEM-resistant cancer stem cells secreted through exosomes miR-210 induced drug resistance through mTOR signaling potentiation. (E) The knockdown of EPHA2 in drug-resistant cells decreased their efficiency in transmitting GEM resistance. Created with BioRender.com.