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. 2020 Feb 1;12(2):332. doi: 10.3390/cancers12020332

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© 2020 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 (http://creativecommons.org/licenses/by/4.0/).

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Sorafenib and regorafenib regulate the BCL-2 profile differently, sharing mitochondrial dependence but a distinctive therapeutic approach. (A) Transcriptomic analysis of genes related with liver cancer in BCLC9 tumors from nude mice treated for three weeks with vehicle (C1-3), sorafenib (S1-3), or regorafenib (R1-3). (B) mRNA expression of different BCL-2 proteins from treated tumors (C1-4, S1-4, and R1-4). Differences in the mRNA pattern are highlighted with yellow squares. (C) Cancer therapy may increase anti-apoptotic BCL-2 proteins avoiding cell death but mito-priming the cells to BH3-mimetics. Resistant hepatoma cells treated with compounds targeting BCL-2 proteins may release BH3-only proteins to bind BAX/BAK and trigger apoptotic cell death.