Background:

Hepatocellular carcinoma (HCC) is the most common malignant tumors, accounting for most of the adult primary liver cancer. Herein, we aimed to analyze the expression of long non-coding RNA-T cell leukemia/lymphoma 6 (lncRNA-TCL6) in HCC and elucidate its mechanism involved in the HCC progression. Methodse performed RNA extraction and quantitative real-time polymerase chain reaction assays, spheroid formation assays, flow cytometry and western blot assays to assess the effect of TCL6 on the liver CSCs marker CD133 expression rate, sphere-forming ability of liver stem cells, and the relationship between TCL6 expression and stem cell factor (TP53, P21, CD44, KLF4, OCT4, Nanog, and Sox2). In addition, we used a dual luciferase assay to verify the relationship between miR-106a-5p and TP53.ResultsKnockdown of TCL6 expression significantly improved the CD133 expression rate and the liver stem cells sphere-forming ability in HCC, while TCL6 overexpression in HCC showed the opposite effect. Knockdown of TCL6 upregulated the KLF4mRNA expression, while TCL6 overexpression in HCC inhibited the TP53 and CDKN1A expression. Western blot assays showed that TCL6 expression was positively correlated with TP53 and P21, while negatively correlated with stem cell factor. Dual luciferase assay showed that TP53 was a target of miR-106a-5p.ConclusionResults suggested that reprogramming-related TCL6 may be a novel tumor suppressor gene in HCC, which inhibits the self-renewal of liver CSCs, in part by promoting the TP53 expression.