Fig. 2

LSD1 maintains the stemness of LCSCs and enhances cell radioresistance by interacting with HOTAIR. A The expression of LSD1 in liver cancer tissues was analyzed based on TCGA database. LIHC, liver hepatocellular carcinoma. The red box plots represent tumor samples and the gray box plots represent normal samples. *p < 0.01 compared with normal samples. B Correlation between the expression of LSD1 and the overall survival of patients with liver cancer. The red line indicates the liver cancer patients with high expression of LSD1, and the blue line indicates liver cancer patients with low expression of LSD1. The upper right is the significant p value and legend. C The expression of LSD1 in adjacent normal tissues and liver cancer tissues, as measured by RT-qPCR, normalized to GAPDH. *p < 0.05 compared with adjacent normal tissues. D The silencing and overexpression efficiency of LSD1 was detected by Western blot, normalized to GAPDH. E The effect of LSD1 depletion or overexpression on LCSCs stemness, as measured by microsphere formation assay. *p < 0.05 compared with shCtl-treated LCSCs, #p < 0.05 compared with oeCtl-treated LCSCs. F The colony formation ability of LCSCs with LSD1 depletion or overexpression after treatment with 6 Gy X-ray irradiation, as examined by clonogenic assay. *p < 0.05 compared with shCtl-treated LCSCs, #p < 0.05 compared with oeCtl-treated LCSCs. G Interaction between HOTAIR and LSD1 assessed by RIP assay. The relative enrichment on the Y-axis represents IP-LSD1/IgG. *p < 0.05 compared with the IgG group. The experimental data were summarized as mean ± standard deviation. Data between cancer tissues and adjacent normal tissues were compared by paired t test, and those between the other two groups were compared by unpaired t test. The data comparison between multiple groups was performed by one-way ANOVA with Tukey’s post-hoc test. Cellular experiments were repeated three times