Fig. 8. BRAFV600E promotes CXCLs level and MDSCs infiltration through TBX3-regulated pathway.
a Levels of CXCLs in PTC cells underwent PLX4032 or SCH772984 treatment were checked by RT-qPCR. b Levels of CXCLs in K1 cells stably over-expressing control Vector or BRAFV600E and subsequently infected with lentiviruses expressing TBX3 shRNAs were analyzed by RT-qPCR. c, d IHC staining in PTC samples with BRAFWT or BRAFV600E paired with adjacent normal tissues. Representative images were shown (c), and the scores of the stained sections were plotted (d), n = 30 normal tissues, n = 66 grade low PTC tissues, and n = 44 grade high PTC tissues. Scale bars, 100μm. e Scatter diagrams of TBX3, CXCL1, CXCL2 and CXCL8 protein levels in BRAFWT (n = 45) and BRAFV600E (n = 65) PTC tissues. f A proposed model of the mechanism of re-activation of TBX3 by BRAF/MAPK constitutive activation leading to immune-suppression by recruiting MDSCs into tumor microenvironment and the rational of combination therapy using PLX4032 and SB265610 or anti-Gr-1 to treat thyroid cancer. n = 3 biological independent samples (a, b). Data are shown as the mean ± s.d. (a, b, d, e). P values were calculated by unpaired two-tailed Student’s t test (a, b, d, e). Statistical source data are provided in Source Data.