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. 2022 Jun 7;12:904327. doi: 10.3389/fonc.2022.904327

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Copyright © 2022 Voisin, Nicole, Gratio, Chassac, Mansour, Rebours, Couvelard and Couvineau

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.

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Histological analysis of resected tumors from Run 02 experiments. (A) OX1R expression and caspase-3 activation in gemcitabine-chemoresistant AsPC-1 tumors (gem^R) treated with PBS (Control), OxA (OxA), and gemcitabine (gem). (B) OX1R expression and caspase-3 activation in Nab-paclitaxel-chemoresistant AsPC-1 tumors (pacli^R) treated with PBS (Control), OxA (OxA), and Nab-paclitaxel (pacli). (C) OX1R expression and caspase-3 activation in 50 days OxA-treated tumors (OxA) treated with PBS (control) and OxA (OxA). (D) OX1R expression and caspase-3 activation in gemcitabine-chemoresistant tumors obtained by xenografting of 50 days gemcitabine-treated PDAC15 cells (gem^R) treated with PBS (control), OxA (OxA), and gemcitabine (gem). (E) Cell viability determination of spheroids developed with parental AsPC-1, gemcitabine-resistant, and Nab-paclitaxel-resistant AsPC-1 cells isolated in Run 02 experiment. Magnification was 40× (OX1R expression) and 20× (caspase-3 activation).