Schematic representation of possible anticancer mechanisms of MM-129. 1: BTK inhibition; 2: phosphatidylserine (PS) externalisation; 3: loss of mitochondrial membrane potential; 4: activation of extrinsic pathway of apoptosis; 5: the activation of internal (mitochondrial) apoptosis; 6: activation of executive caspases. The schematic illustration was created in Adobe Photoshop and Photophea software. Akt: protein kinase B; Apaf-1: apoptotic protease activating factor 1; β-catenin: protein responsible for transduction; Bak: Bcl-2 homologous antagonist/killer; Bax: Bcl-2-associated X protein; Bcl-2: antiapoptotic protein; Bid: Bax-like BH3 protein; tBid: truncated BID; BTK: Bruton’s tyrosine kinase; EGF: epidermal growth factor; FADD: Fas-associated death domain protein; IFNγ: interferon gamma; JAK2: non-receptor tyrosine kinase; mTOR: mammalian target of rapamycin; PDGF: platelet-derived growth factor; PI3K: phosphoinositide 3-kinases; PIP3: phosphatidylinositol-3,4,5-triphosphate; PH: pleckstrin homology domain; STAT: signal transducer and activator of transcription; Wnt: family of secreted lipid-modified signalling glycoproteins.
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