BarH 样同源框 2 (BARX2) 已被确定在多种癌症的发展中发挥关键作用。同时，BARX2可能是肝细胞癌（HCC）患者的独立预后生物标志物。然而，BARX2 在 HCC 中的调节作用仍不清楚，需要揭开。在本研究中，通过实时定量 PCR (qRT-PCR) 以及蛋白质印迹评估了 BARX2 和 N-乙酰半乳糖胺基转移酶 4 (GALNT4) 的表达。此外，分别通过CCK-8、集落形成、伤口愈合、Transwell和管形成实验评估细胞增殖、迁移、侵袭和血管生成的能力。通过流式细胞术分析测定细胞凋亡。 BARX2和GALNT4之间的结合关系由JASPAR网站预测，并使用染色质免疫沉淀（ChIP）和荧光素酶报告测定进行验证。研究发现，BARX2在HCC细胞系中表达减少，而其过表达则极大地抑制HuH7和MHCC97-H细胞中的细胞增殖、迁移、侵袭和血管生成，并促进细胞凋亡。 BARX2可以结合GALNT4启动子并正向调节GALNT4的表达。此外，GALNT4缺陷部分消除了BARX2对HCC进展的抑制作用。总之，本研究强调 BARX2 可能有望作为潜在的治疗靶点，促进针对 HCC 的新型治疗策略的开发。© 2023。作者获得 Springer Science Business Media, LLC 的独家许可，施普林格自然的一部分。

BarH-like homeobox 2 (BARX2) has been identified to play a key role in the development of multiple cancers. Meanwhile, BARX2 may be an independent prognostic biomarker for patients suffering from hepatocellular carcinoma (HCC). Nevertheless, the regulatory role of BARX2 in HCC is still unclear and needs to be unveiled. In this study, the expressions of BARX2 and N-acetylgalactosaminyltransferase 4 (GALNT4) were evaluated by quantitative real-time PCR (qRT-PCR) as well as western blot. Besides, the abilities of cells to proliferate, migrate, invade, and angiogenesis were assessed with CCK-8, colony formation, wound-healing, Transwell, and tube formation assays, separately. Cell apoptosis was determined by flow cytometry analysis. The binding relationship between BARX2 and GALNT4 was predicted by JASPAR website and verified using Chromatin immunoprecipitation (ChIP) and luciferase report assay. It was discovered that BARX2 was reduced in HCC cell lines, while its overexpression greatly repressed cell proliferation, migration, invasion, and angiogenesis and promoted cell apoptosis in HuH7 and MHCC97-H cells. BARX2 could bind to GALNT4 promoter and positively regulate GALNT4 expression. In addition, GALNT4 deficiency partly abolished the inhibitory effects of BARX2 on the progression of HCC. In summary, this study highlights that BARX2 may hold promise for serving as a potential therapeutic target, facilitating the development of a novel therapeutic strategy against HCC.© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.