Fig 2: Schematic diagram of cisplatin resistant lung cancer cells promoted M2 polarization of tumor-associated macrophages via the Src/CD155/MIF functional pathway. Thus, kinase inhibitors such as dasatinib may be of potential for treating cisplatin-resistant lung cancer by targeting both tumor and the tumor microenvironment

Fig 3: CD103 + DCs are critical for effective anti-tumor responses to RT combined with anti-TIGIT therapy. a. Frequency of CD103 + DCs among total myeloid cells infiltrating MC38, B16-F10, and LLC tumor models. Myeloid cells were gated on CD11b + and/or CD11c + cells within CD45 + cells. b. Quantification of CD155 on CD103 + DCs purified from MC38 TdLNs, non-draining LNs, and healthy mouse LNs on day 10 following tumor challenge. The gating strategy is shown in Fig. S9. c. MC38 tumor-bearing WT or BATF3-/- mice were treated with RT plus anti-TIGIT therapy or RT alone on day 10 after the tumor challenge. Data are shown as mean ± SEMs (standard errors of the mean) for two independent experiments (n = 4–5). (d-e). The production of IFN-? (interferon gamma) and TNF-a (tumor necrosis factor alpha) by CD8 + T-cells in tumor tissues d and TdLNs e was analyzed herein. f. WT and BATF3.-/- mice were inoculated with MC38 cells and treated with RT and anti-TIGIT therapy as described in Fig. 3a. Moreover, 200 µg of anti-CD8 monoclonal antibodies (mAb) was administered as described in Fig. 5a. Tumor growth was monitored after RT. Data are shown as means ± SEM (standard errors of the mean) of two independent experiments (n = 5). *p < 0.05; ***p < 0.001; ****p < 0.0001. BATF3, basic leucine zipper transcription factor ATF-like 3; DCs, dendritic cells; LNs, lymph nodes; mAb, monoclonal antibodies; NS, not statistically significant; RT, radiotherapy; TdLNs, tumor draining lymph nodes; TIGIT, T cell immunoreceptor with immunoglobulin and ITIM (immunoreceptor tyrosine-based inhibitory motif) domains; WT, wild type

Fig 4: A heat map presenting data on 20 immune checkpoints from a TMA containing 124 GC patient samples.The abscissa represents the patient number of 124 patients in the TMA, and the ordinate represents the expression of LSECtin, VISTA, PD-L1, IDO, TIM-3, TNFRSF14, B7M4, CEACAM1, NECTIN2, CD44, CD155, ADENOSINE, TLR4, HMGB1, SIGLEC6, FAS-L, SIGLEC15, CD73, Galectin-9 and PD-L2.

Fig 5: Dasatinib treatment decreased CDDP-resistance and stemness of NSCLC cells. a Comparative MTT assay showed that when A549R and H460R cells were first treated with dasatinib (1 µM, 24 h) followed by CDDP treatment demonstrated an increased sensitivity towards CDDP. b Tumor sphere formation assay showed that dasatinib treatment (10 µM) significantly inhibited the formation of tumor spheres in both A549R and H460R cells. c Flow cytometry analysis of CD133+ cells. Dasatinib treatment dose-dependently decreased the percentage of CD133+ cell population in both H460R and A549R cells. The bar graph on the right shows the comparative level of CD133+ cell population (from the flow cytometric analysis on the left) under different concentration of dasatinib treatment. *P < 0.05 as compared to the control. d Expression profiling of A549R and H460R post dasatinib treatment (5 µM, 24 h). The expression of pro-tumorigenesis molecules, Src, CD155 and MIF, cancer stemness molecules, Notch1 and ß-catenin was all significantly suppressed under dasatinib treatment