Fig. 7: Schematic illustration of the proposed model. | Cell Death & Disease

Fig. 7: Schematic illustration of the proposed model.

From: CXCR2 expression on granulocyte and macrophage progenitors under tumor conditions contributes to mo-MDSC generation via SAP18/ERK/STAT3

Fig. 7: Schematic illustration of the proposed model.

The level of CXCL1 and CXCL2 was very low under normal physiological conditions, but the level was greatly increased under tumor conditions. The increased CXCL1 and CXCL2 under tumor conditions binds to its receptor CXCR2 on GMPs. In this case, the GMPs expressed low level of SAP18 resulting in decreasing the binding of mSin3A to the promoter of HRAS and PI3Kγ, which enhanced the transcription of HRAS and PI3Kγ in the GMPs. The increased expression of HRAS and PI3Kγ promoted the phosphorylation of ERK1/2 and subsequently activated STAT3 signaling pathway to promote mo-MDSCs accumulation

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