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. 2023 Feb 17;24(4):4053. doi: 10.3390/ijms24044053

Figure 2.

Figure 2

Predicted mechanism of action of MM compounds: MM compounds may act as BTK, PI3K-AKT-mTOR, and PD-L1 inhibitors that reduce cell survival and trigger apoptosis in a cytotoxic T-cell-dependent mechanism. Inhibition of mTOR kinase leads to up-regulation of PD-L1 expression. Increased expression of PD-L1 may result from the accumulation of DNA damage and activation of ATM/ATR/CHK1 and JAK/STAT/IRF signaling pathways. DNA damage leads to the up-regulation of TP53 tumor suppressor and induction of pro-apoptotic proteins including BAK and BAX involved in the intrinsic apoptosis pathway associated with MMP changes and increased production of P21 that works as an inhibitor of CDK2. AKT—RAC-alpha serine/threonine-protein kinase; ATM/ATR—serine-protein kinase ATM/ATR; BAX/BAK—pro-apoptotic protein BAX/BAK; BTK—tyrosine-protein kinase BTK; CDK2—cyclin-dependent kinase 2; CHK1—serine/threonine-protein kinase CHK1; DSB—double-strand break; IRF1—interferon regulatory factor 1; JAK—tyrosine-protein kinase JAK; MMP—mitochondrial membrane potential; mTOR—serine/threonine-protein kinase mTOR; PI3K—phosphatidylinositol-4,5-bisphosphate 3-kinase; PD-L1—programmed cell death 1 ligand 1; RTK—receptor tyrosine kinase; STAT—signal transducer and activator of transcription; TP53—cellular tumor antigen p53; γH2AX—phosphorylated histone protein H2AX.