Fig. 1

HOTAIR expression is increased in liver cancer tissues and LCSCs, which links to stemness maintenance and radioresistance of LCSCs. A A Volcano map of the gene expression between CD13+CD133+ liver cancer cell subsets and negative liver cancer cell subsets based on the RNA-seq data. Red indicates highly expressed genes while green indicates poorly expressed genes. B The expression of HOTAIR in liver cancer and normal tissue samples in TCGA database (p = 0.03). C Correlation between the expression of HOTAIR and the progression free survival of patients with liver cancer. D The expression of HOTAIR in normal and liver cancer tissues measured by RT-qPCR, normalized to GAPDH. *p < 0.05 compared with adjacent normal tissues. E Silencing and overexpression efficiency of HOTAIR determined by RT-qPCR in Hep3B and Huh7 CSCs. *p < 0.05 compared with Hep3B and Huh7 CSCs treated with shCtl, # p < 0.05 compared with Hep3B and Huh7 CSCs treated with oeCtrl. F The effect of HOTAIR silencing or overexpression on the stemness maintenance of LCSCs, as detected by microsphere formation assay. G The colony formation ability of LCSCs after 6 Gy X-ray irradiation after HOTAIR silencing or overexpression, as examined by clonogenic assay. *p < 0.05 compared with Hep3B and Huh7 CSCs treated with shCtl, # p < 0.05 compared with Hep3B and Huh7 CSCs treated with oeCtrl. Data were represented 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 in triplicate