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. 2022 Apr 30;10(5):1038. doi: 10.3390/biomedicines10051038

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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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Schematic diagram depicting TKI-activated NFKB2-MIF/CXCLs-CXCR2 compensation pathways responsible for the survival and proliferation of AML blasts. After TKI treatment, cytotoxicity-induced injury signals might directly activate the non-canonical NFKB2 (P100/P52) pathway to release more MIF, CXCL5, CXCL8 and other tumor-promoting cytokines. MIF might act as an autocrine signal to initiate the survival mechanism* through MIF-CD74/CD44 pathways. Meanwhile, MIF-CXCR2, CXCL5-CXCR2 and CXCL8-CXCR2 pathways might be responsible for cell proliferation by activating CDK4/CYCLIN E-based transition from G1 to S phase of the cell cycle progression. * pBAD-BCL2: Phosphorylation of BAD has been restored by PIM family compensation pathways to prevent its binding to BCL-2, allowing blasts to survive the TKI treatment. Red color indicates the key molecules in this study.