Prognostic Significance of Actinin-4 Protein Expression and Gene Amplification in Endometrial Carcinoma

肌动蛋白-4蛋白表达和基因扩增在子宫内膜癌中的预后意义

阅读:1

Abstract

OBJECTIVE: This study aimed to investigate the clinical significance of actinin-4 in endometrial carcinoma. Actinin-4, an actin-binding protein involved in cytoskeletal dynamics, has been implicated in the progression of various cancers; however, its precise role in endometrial carcinoma is not fully understood. This research sought to evaluate actinin-4 protein expression and gene amplification and correlate these findings with clinicopathological parameters and patient survival to determine its prognostic value. METHODS: A retrospective analysis was conducted on endometrial carcinoma patients who underwent surgical resection. Actinin-4 protein expression was assessed using immunohistochemical staining (IHC), and ACTN4 gene amplification was evaluated by fluorescence in situ hybridization (FISH). The intensity of actinin-4 staining was graded, and gene amplification of ACTN4 was defined using the ACTN4/CEP19 ratio. Statistical analysis, including Kaplan-Meier survival analysis and Cox proportional hazards modeling, was performed to correlate actinin-4 expression with clinicopathological features and survival outcomes. RESULTS: Overexpression of actinin-4 protein by IHC was significantly associated with advanced clinical stage and histological subtypes. While no significant difference was observed in overall survival (OS), patients with high actinin-4 IHC demonstrated significantly poorer progression-free survival (PFS). ACTN4 gene amplification by FISH was significantly associated with poorer prognosis for both OS and PFS compared to the group without amplification. CONCLUSION: This study suggests that actinin-4 plays a role in the progression of endometrial carcinoma, particularly influencing tumor aggressiveness and progression-free survival.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。