Fig. 1

Local AngII in tumor microenvironment is involved in immune escape of tumor cells. a The influence of AngII-receptor blockers on 4T1 tumor growth in syngeneic BALB/c mice; candesartan (cand, 5mg/kg, i.p.; starting at day 5 after cell injection, daily ) for AT1R and PD123319 (5mg/kg, i.p.; starting from day 5 after cell injection, every other day) for AT2R, n=5. b The influence of AngII-receptor blockers on 4T1 cells proliferation in vitro as detected by MTT assay; candesartan (10μm/well) and PD123319 (10μm/well). c The influence of Ang II-receptor blockers on 4T1 tumor growth in T-cell immunodeficient BALB/c nude mice, n=5. d The expression of AGT, a precursor of AngII, was silenced in 4T1 cells and CT26 cells by shRNA. Hypoxia remarkably induced generation of Ang II in 4T1 and CT26 cells as detected by ELISA. AGT-silencing greatly decreased Ang II levels, especially under hypoxic condition. Data are presented as mean±SEM, n=3. e AGT silencing did not influence cell-proliferation of 4T1 cells in vitro as detected by MTT assay. f AGT silencing obviously inhibited tumor growth of 4T1cells in BALB/c mice comparing to negative control, and the depletion of CD8⁺ T cells in mice by in vivo administration of monoclonal antibody against CD8 greatly attenuated this effect (n=6). Ns, no significance; *, P < 0.05; **, P < 0.01