Department of General Surgery, The First Affiliated Hospital of Anhui Medical University, Hefei, China.
Department of Pathology, The First Affiliated Hospital of Anhui Medical University, Hefei, China.
J Cell Mol Med. 2024 Mar;28(6):e18164. doi: 10.1111/jcmm.18164.
Ubiquitin A-52 residue ribosomal protein fusion product 1 (UBA52) has a role in the occurrence and development of tumours. However, the mechanism by which UBA52 regulates hepatocellular carcinoma (HCC) tumorigenesis and progression remains poorly understood. By using the Cell Counting Kit (CCK-8), colony formation, wound healing and Transwell assays, we assessed the effects of UBA52 knockdown and overexpression on the proliferation and migration of HCC cells in vitro. By establishing subcutaneous and metastatic tumour models in nude mice, we evaluated the effects of UBA52 on HCC cell proliferation and migration in vivo. Through bioinformatic analysis of data from the Gene Expression Profiling Interactive Analysis (GEPIA) and The Cancer Genome Atlas (TCGA) databases, we discovered that UBA52 is associated with autophagy. In addition, we discovered that HCC tissues with high UBA52 expression had a poor prognosis in patients. Moreover, knockdown of UBA52 reduced HCC cell growth and metastasis both in vitro and in vivo. Mechanistically, knockdown of UBA52 induced autophagy through EMC6 in HCC cells. These findings suggest that UBA52 promoted the proliferation and migration of HCC cells through autophagy regulation via EMC6 and imply that UBA52 may be a viable novel treatment target for HCC patients.
泛素 A-52 残基核糖体蛋白融合产物 1（UBA52）在肿瘤的发生和发展中具有作用。然而，UBA52 调节肝细胞癌（HCC）肿瘤发生和进展的机制仍知之甚少。通过使用细胞计数试剂盒（CCK-8）、集落形成、划痕愈合和 Transwell 分析，我们评估了 UBA52 敲低和过表达对 HCC 细胞体外增殖和迁移的影响。通过在裸鼠中建立皮下和转移肿瘤模型，我们评估了 UBA52 对 HCC 细胞体内增殖和迁移的影响。通过对基因表达谱交互式分析（GEPIA）和癌症基因组图谱（TCGA）数据库中数据的生物信息学分析，我们发现 UBA52 与自噬有关。此外，我们发现 UBA52 高表达的 HCC 组织患者预后不良。此外，UBA52 的敲低降低了 HCC 细胞在体外和体内的生长和转移。在机制上，UBA52 通过 HCC 细胞中的 EMC6 诱导自噬。这些发现表明，UBA52 通过 EMC6 调节自噬促进 HCC 细胞的增殖和迁移，并暗示 UBA52 可能是 HCC 患者的一种可行的新治疗靶点。
