Fig. 5: STAT1 mediates CXCL7-induced PHGDH transcription and chemotherapy resistance. | Cell Death & Disease

Fig. 5: STAT1 mediates CXCL7-induced PHGDH transcription and chemotherapy resistance.

From: Chemotherapy-induced macrophage CXCL7 expression drives tumor chemoresistance via the STAT1/PHGDH-serine metabolism axis and SAM paracrine feedback to M2 polarization

Fig. 5

A GSEA analysis illustrating the correlation between CXCL7 and the interferon signaling pathway. B Predicted STAT1-binding sequences in the PHGDH promoter region using the JASPAR database. C The correlationship between STAT1 and PHGDH mRNA expression. D ChIP-qPCR results showing STAT1 enrichment at the PHGDH promoter. E Luciferase reporter assay results demonstrating PHGDH promoter activity in response to CXCL7 treatment with or without JAK1 inhibition. F Effects of JAK1 inhibition on PHGDH mRNA expression following CXCL7 treatment. G Western blot analysis of p-JAK1, JAK1, p-STAT1, STAT1, PHGDH, and IRF9 protein levels in cells treated with CXCL7 with or without JAK1 inhibition. H Cell viability assessment for cell treatment with CXCL7, following PHGDH inhibition or JAK1 inhibition. I Effects of PHGDH or JAK1 inhibition on tumor growth in mice with CXCL7-overexpressing cell. J IHC analysis of p-STAT1, PHGDH, and CD206 expression, along with TUNEL staining for apoptosis, in CXCL7-overexpressing tumors treated with PHGDH or JAK1 inhibitor (scale bar for IHC, 50 μm; scale bar for TUNEL, 10 μm). All data are presented as mean ± SD. *P < 0.05; n.s.not significant.

Back to article page