Fig. 2: Deficiency of mGluR4 delays tumor progression and prolongs mouse survival.

A The orthotopic liver tumor surveillance of Hepa1-6BL in WT and Grm4-/- mice was quantified by tumor-bearing liver weight (n = 14), B the number of liver tumor nodules (n = 14), C spontaneous lung metastases (n = 10), D the level of ALT and AST in serum (Naïve n = 8, WT n = 10, Grm4-/- n = 10), E and survival of mice (WT n = 21, Grm4-/- n = 15). F Subcutaneous tumor growth, (G) weight statistics of Hepa1-6BL in WT and Grm4-/- mice on day 16 (n = 7). H–J Subcutaneous tumor growth of (H) MC38-OVAdim (n = 6), (I) SM1WT1 (WT n = 7, Grm4-/- n = 8) and (J) MCA1956 (WT n = 8, Grm4-/- n = 7) cells in WT and Grm4-/- mice (Statistics of tumor rejection rate in the groups was shown in parentheses). K, L Lung metastases of (K) MC38 (n = 6) and (L) B16F10 (n = 7) cells in WT and Grm4-/- mice. M MC38-OVAdim subcutaneous tumor growth in WT and Grm4-/- mice after BM transplantation (WT BM → WT n = 9, WT BM → Grm4-/- n = 11, Grm4-/- BM → WT n = 10, Grm4-/- BM → Grm4-/- n = 10). N–P SM1WT1 subcutaneous tumor growth in WT and Grm4-/- mice after treated intraperitoneally with (N) cIg/anti-IFNγ (WT cIg n = 8, Grm4-/- cIg n = 6, WT α-IFNγ n = 6, Grm4-/- α-IFNγ n = 6), (O) cIg/anti-CD8β (WT cIg n = 7, Grm4-/- cIg n = 6, WT α-CD8β n = 6, Grm4-/- α-CD8β n = 7), (P) cIg/anti-ASGM1 (WT cIg n = 6, Grm4-/- cIg n = 7, WT α-ASGM1 n = 6, Grm4-/- α-ASGM1 n = 7). Data is shown as mean ± SEM. Statistical significance was determined by unpaired t-test two-tailed (A–D, G, K, L), Mann-Whitney test (two-tailed) (F, H, I, J), one-way ANOVA (two-tailed) with Tukey’s multiple comparisons test (M–P) or log-rank Mantel-Cox test (two-sided) (E). All biological experiments were repeated at least three times. Source data are provided as a Source Data file.