Fig 1: Sorafenib treatment increases intratumoral hypoxia and alters HCC microenvironment towards an immune-resistant state in mouse models.A, B orthotopic Hepa 1-6 and Hepa 1c1c7 tumors were treated with sorafenib or vehicle control for three weeks, then collected protein lysates for western blot (A) or tissue samples for Pimonidazole staining (B). C, D infiltrating immune cells in orthotopic Hepa 1-6 and Hepa 1c1c7 tumors treated with sorafenib or vehicle control were evaluated by flow cytometry. CD3+CD4+CD25+FoxP3+ Treg, CD11b+Gr-1−Ly6C−F4/80+ TAM, CD11b+Gr-1+Ly6CintLy6G+ PMN-MDSC, CD11b+Gr-1+Ly6ChighLy6G- M-MDSC and CD3+CD4-CD8+ Cyto T cells were evaluated. E relative expression of PD-L1, TGFB1, IL10, and IL13 in orthotopic Hepa 1-6 and Hepa 1c1c7 tumors was evaluated by qRT-PCR. F protein expression of PD-L1 in orthotopic Hepa 1-6 and Hepa 1c1c7 tumors was evaluated by western blot. All assays were done with at least three repeats. Data were shown as mean ± s.d., *P < 0.05.
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