Supplementary Data from NOTCH Signaling via WNT Regulates the Proliferation of Alternative, CCR2-Independent Tumor-Associated Macrophages in Hepatocellular Carcinoma

Abstract

<p>Figure S1: Experimental design, Figure S2: LyzM-Cre-mediated RBPj cKO suppressed the growth of subcutaneous LLC tumors, Figure S3: LyzM-Cre-mediated RBPj cKO promoted the growth of orthotopic HCC tumors, Figure S4: kclTAMs dominated TAM populations promoting HCC growth, Figure S5: RBPj cKO led to increased proliferation of kclTAMs without influencing apoptosis in hepatic Hepa1-6 tumors, Figure S6: RBPj cKO did not affect the proliferation capacity of monocytes in vitro, Figure S7: RBPj cKO promoted the growth of hepatic Hepa1-6 tumors independent of CCR2,Figure S8: Notch signaling negatively regulated the activation of Wnt/β-catenin signaling and the proliferation of kclTAMs, Figure S9: Blocking Wnt signaling inhibited the growth of hepatic Hepa1-6 tumors, Figure S10: Knockdown of β-catenin repressed the proliferation of RBPj-deficient KCs, Figure S11: RBPj cKO promoted kclTAM proliferation and hepatic tumor growth through β-catenin-dependent Wnt signaling, Figure S12: RBPj cKO promoted the hepatic metastasis but suppressed lung metastasis, Figure S13: A model depicting the role of Notch signaling in TAM subsets regulating hepatic tumor growth and metastasis in liver, Table S1: Clinical data of 44 HCC patients involved in this study, Table S2: Antibodies used in this study, Table S3: Primers and oligonucleotides used in this study</p>