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Fig. 5 | BMC Cancer

Fig. 5

From: Identification of CEACAM5 as a stemness-related inhibitory immune checkpoint in pancreatic cancer

Fig. 5

Association of CEACAM5 expression with and sensitivity to small molecular inhibitors. A-H Pearson’s correlation between CEACAM5 expression and drug sensitivity to (A) Niclosamide, an inhibitor of STAT3 signalling, (B) Palmostatin B, an inhibitor of acyl-protein thioesterase 1, (C) SB-225002, an inhibitor of chemokine receptor 2, (D) SGX-523, an inhibitor of MET, (E) Axitinib, an inhibitor of VEGFRs, c-KIT, and PDGFR α and β, (F) SCH-79797, an antagonist of proteinase-activated receptor 1, (G) Sorafenib, an inhibitor of BRAF, CRAF, and VEGFR2, and (H) 3-CL-AHPC, a binder of nuclear receptor SHP. I-P Pearson’s correlation between CEACAM5 expression and drug sensitivity to (I) MK-2206, an inhibitor of AKT1, (J) BYL-719, an inhibitor of PI3K catalytic subunit α, (K) BRD-K85133207, an inhibitor of HDAC1, (L) Semagacestat, an inhibitor of γ-secretase, (M) PDMP, an inhibitor of ceramide glucosyltransferase, (N) Vorapaxar, an antagonist of proteinase-activated receptor 1, (O) Linsitinib, an inhibitor of insulin-like growth factor 1 receptor and insulin receptor, and (P) PF-543, an inhibitor of sphingosine kinase-1

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