Krüppel-like factor (KLF) has a role in the occurrence, development and metabolism of cancer. We aimed to explore the role and potential molecular mechanism of KLF13 in the growth and migration of liver cancer cells.

The expression of KLF13 in hepatocellular carcinoma (HCC) tissues was higher than that in normal tissues according to analysis of The Cancer Genome Atlas (TCGA) database. Lentiviral plasmids were used for overexpression and plasmid knockdown of KLF13. Real-time quantitative polymerase chain reaction (qPCR) and western blotting were used to detect mRNA and protein expression in HCC tissues and cells. Cell counting kit-8 (CCK-8), colony formation, cell migration and invasion, and flow cytometry assays were used to assess the in vitro function of KLF13 in HCC cells. The effect of KLF13 on xenograft tumor growth in vivo was evaluated. The cholesterol content of HCC cells was determined by an indicator kit. A dual-luciferase reporter assay and chromatin immunoprecipitation sequencing (ChIP-seq) revealed the binding relationship between KLF13 and HMGCS1.

The expression of KLF13 was upregulated in HCC tissues and TCGA database. KLF13 knockdown inhibited the proliferation, migration and invasion of HepG2 and Huh7 cells and increased the apoptosis of Huh7 cells. The opposite effects were observed with the overexpression of KLF13 in SK-Hep1 and MHCC-97H cells. The overexpression of KLF13 promoted the growth of HCC in nude mice and KLF13 transcription promoted the expression of HMGCS1 and the biosynthesis of cholesterol. KLF13 knockdown inhibited cholesterol biosynthesis mediated by HMGCS1 and inhibited the growth and metastasis of HCC cells.

KLF13 acted as a tumor promoter in HCC by positively regulating HMGCS1-mediated cholesterol biosynthesis.

Krüppel样因子（KLF）在癌症的发生、发展和代谢中发挥作用。我们旨在探讨KLF13在肝癌细胞生长和迁移中的作用和潜在的分子机制。

根据癌症基因组图谱 (TCGA) 数据库的分析，KLF13 在肝细胞癌 (HCC) 组织中的表达高于正常组织。慢病毒质粒用于 KLF13 的过表达和质粒敲低。使用实时定量聚合酶链反应 (qPCR) 和蛋白质印迹检测 HCC 组织和细胞中的 mRNA 和蛋白质表达。细胞计数试剂盒 8 (CCK-8)、集落形成、细胞迁移和侵袭以及流式细胞术测定用于评估KLF13 在 HCC 细胞中的体外功能。KLF13对体内异种移植肿瘤生长的影响被评估。HCC 细胞的胆固醇含量由指示剂试剂盒测定。双荧光素酶报告分析和染色质免疫沉淀测序 (ChIP-seq) 揭示了 KLF13 和 HMGCS1 之间的结合关系。

KLF13 的表达在 HCC 组织和 TCGA 数据库中上调。KLF13敲低抑制了HepG2和Huh7细胞的增殖、迁移和侵袭，增加了Huh7细胞的凋亡。在 SK-Hep1 和 MHCC-97H 细胞中 KLF13 的过表达观察到相反的效果。KLF13的过表达促进了裸鼠HCC的生长，KLF13的转录促进了HMGCS1的表达和胆固醇的生物合成。KLF13敲低抑制了HMGCS1介导的胆固醇生物合成，抑制了HCC细胞的生长和转移。

KLF13 通过正向调节 HMGCS1 介导的胆固醇生物合成，在 HCC 中充当肿瘤启动子。