Fig. 7

JMJD6 inhibitor SKLB325 represses the LCSC stemness and relieves cell radioresistance. A The expression of HOTAIR, JMJD6 and LSD1 in Hep3B and Huh7 CSCs in response to JMJD6 inhibitor SKLB325 determined by RT-qPCR, normalized to GAPDH. B The expression of HOTAIR and MAPK1 in Hep3B and Huh7 CSCs in response to JMJD6 inhibitor SKLB325 determined by RT-qPCR, normalized to GAPDH. C The expression of Sox2 and Oct2 in Hep3B and Huh7 CSCs in response to JMJD6 inhibitor SKLB325 determined by RT-qPCR, normalized to GAPDH. D The difference of cell stemness after SKLB325 treatment, as detected by microsphere formation assay. E The impact of SKLB325 on colony formation ability in response to SKLB325 treatment, as detected by clonogenic assay. F The diameter of xenografts tumors in mice with SKLB325 treatment. G The tumor volume of xenografted tumors. H, ERK2 (MAPK1) expression in the tumor tissues of mice in response to JMJD6 inhibitor SKLB325 measured by immunohistochemistry. I The expression of HOTAIR in the tumor tissues of mice in response to JMJD6 inhibitor SKLB325 determined by RT-qPCR, normalized to GAPDH. J Ki-67 staining and TUNEL staining were adopted to examine cell proliferation and apoptosis in the tumor tissues of mice in response to JMJD6 inhibitor SKLB325. *p < 0.05 compared with DMSO-treated cells or mice. Experimental data were shown as mean ± standard deviation. Results between two groups were compared by unpaired t test