DataSheet_1_RETRACTED: ZNF655 Promotes the Progression of Glioma Through Transcriptional Regulation of AURKA.zip

ObjectivesGlioma has a high degree of malignancy, strong invasiveness, and poor prognosis, which is always a serious threat to human health. Previous studies have reported that C2H2 zinc finger (ZNF) protein is involved in the progression of various cancers. In this study, the clinical significance, biological behavior, and molecule mechanism of ZNF655 in glioma were explored.MethodsThe expression of ZNF655 in glioma and its correlation with prognosis were analyzed through public datasets and immunohistochemical (IHC) staining. The shRNA-mediated ZNF655 knockdown was used to explore the effects of ZNF655 alteration on the phenotypes and tumorigenesis of human glioma cell lines. Chromatin immunoprecipitation (ChIP)-qPCR and luciferase reporter assays were performed to determine the potential mechanism of ZNF655 regulating Aurora kinase A (AURKA).ResultsZNF655 was abundantly expressed in glioma tissue and cell lines SHG-44 and U251. Knockdown of suppressed the progression of glioma cells, which was characterized by reduced proliferation, enhanced apoptosis, cycle repression in G2, inhibition of migration, and weakened tumorigenesis. Mechanistically, transcription factor ZNF655 activated the expression of AURKA by directly binding to the promoter of AURKA. In addition, downregulation of AURKA partially reversed the promoting effects of overexpression of ZNF655 on glioma cells.ConclusionsZNF655 promoted the progression of glioma by binding to the promoter of AURKA, which may be a promising target for molecular therapy.

本研究旨在探讨胶质瘤中ZNF655蛋白的临床意义、生物学行为及其分子机制。通过对公共数据集及免疫组化（IHC）染色的分析，研究了ZNF655在胶质瘤中的表达及其与预后的关系。通过shRNA介导的ZNF655敲低实验，探讨了ZNF655变异对人类胶质瘤细胞系表型和肿瘤发生的影响。采用染色质免疫沉淀（ChIP）-qPCR和荧光素酶报告基因实验，确定了ZNF655调节Aurora激酶A（AURKA）的潜在机制。结果显示，ZNF655在胶质瘤组织和细胞系SHG-44及U251中高表达。敲低ZNF655抑制了胶质瘤细胞的进展，表现为增殖减少、凋亡增强、G2期细胞周期抑制、迁移抑制和肿瘤发生减弱。机制上，转录因子ZNF655通过直接结合AURKA启动子激活AURKA的表达。此外，AURKA的下调部分逆转了ZNF655过表达对胶质瘤细胞的促进作用。结论指出，ZNF655通过结合AURKA启动子促进胶质瘤的进展，这可能是分子治疗的一个有希望的靶点。