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. 2021 Nov 24;11:718636. doi: 10.3389/fonc.2021.718636

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Copyright © 2021 Carlos-Reyes, Muñiz-Lino, Romero-Garcia, López-Camarillo and Hernández-de la Cruz

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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Cellular mechanisms associated with radioresistance. Cytoplasmic membrane, reticulum endoplasmic, and mitochondria are the main organelles where tumor cells assemble a response to develop radioresistance. Radiation can damage the endoplasmic reticulum (ER) homeostatic state and cause ER stress that will favor radioresistance. This last is also supported by mitochondrial alterations, metabolic remodeling, and by an increase in plasma membrane interconnections favoring the formation of cytoplasmic bridges. Cetuximab promotes radioresistance involving ERS pathway IRE1α/ATF6-GRP78. Silencing GRP78 inhibits the cooperative effects of radiotherapy and cetuximab inhibiting DSB repair and autophagy in OPCC. IRE1 promotes radioresistance in HPV-negative OPCC through IL-6 activation. Decreased MPC1 expression favors EMT and promotes radioresistance of cancer.