KAT3B acts as an oncogene in PCa by mediating the succinylation of c-Myc and promoting its stability

Sep 29, 2026

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This study investigates how the lysine acetyltransferase KAT3B, acting as a succinylase, influences prostate cancer (PCa) progression through post-translational succinylation. KAT3B expression was evaluated using qRT-PCR, Western blotting, and immunofluorescence, while protein interactions were tested by immunoprecipitation and co-immunoprecipitation. Functional effects on viability, apoptosis, migration, and invasion were assessed by CCK-8, flow cytometry, and transwell assays. Mechanistically, KAT3B enhances c-Myc succinylation and stability; c-Myc overexpression counteracts KAT3B knockdown. In vivo, KAT3B silencing suppresses tumor growth.

LanguageEnglish

CategoryHealthcare

FormatPDF

Pages9

Reading Time23 min

AccessFree to download

Abstract

Background

Methods

Results

Conclusion

Introduction

Materials and methods

Clinical specimens

Nie et al. World Journal of Surgical Oncology (2026) 24:11 [https://doi.org/10.1186/s12957-025-04068-7](https://doi.org/10.1186/s12957-025-04068-7) World Journal of Surgical Oncology RESEARCH Open Access KAT3B acts as an oncogene in PCa by mediating the succinylation of c-Mycand promoting its stability Wei Nie 1, Shifang Cha2 and Quanwei Fu3* Abstract Background As a form of protein modification, succinylation significantly impacts protein function and helps govern a range of signaling mechanisms. This study was designed to explore the role of KAT3B, functioning as a succinylase, in the context of prostate cancer (PCa) . Methods The expression levels were assessed using quantitative real-time PCR, Western blot, and immunofluorescence staining. To investigate protein-protein interactions, immunoprecipitation assays were performed. The interaction between proteins were confirmed by Co-immunoprecipitation assay. The cell phenotype of PCa cells was analyzed by CCK-8, flow cytometry, and transwell assays. Results We found that KAT3B was over-expressed in PCa tumor tissues and cells. Downregulated KAT3B decreased the viability, migration, and invasion while accelerating the apoptosis of PCa cells. Mechanistically, KAT3B mediated the succinylation of c-Myc, meantime promoted the stability of c-Myc. c-Myc overexpression reversed the role of KAT3B in PCa cells. The in vivo study verified that KAT3B silencing inhibited the growth of PCa cancer tissues. Conclusion Our research indicates that KAT3B was highly expressed in PCa. KAT3B silencing inhibited PCa cell growth and cancer tissues growth by decreasing the succinylation and expression of c-Myc. These findings potentially contribute to novel approaches in diagnosing and treating PCa. Keywords Prostate cancer, KAT3B, C-Myc, Succinylation Introduction Prostate cancer (PCa) is a malignant tumor occurring in the prostate. The disease tends to occur in older men over the age of 65 [1]. Recently, there has been a notable rise in the diagnosis of PCa among men younger than 55 years of age. The incidence of PCa varies greatly by race, *Correspondence: Quanwei Fu [fuqw@163.com](fuqw@163.com) 1PET-CT Center, Citic Huizhou Hospital, Huizhou, China 2Department of Urology, Citic Huizhou Hospital, Huizhou, China 3Medical Office, Citic Huizhou Hospital, Zhongkai Avenue, Huicheng District, Huizhou, Guangdong Province 516006, China familial inheritance, and geographical location [2]. Localized PCa is asymptomatic; however, once symptoms appear, PCa is usually too advanced and incurable. Thus, early screening is particularly important [3]. Moreover, over 10% of patients are diagnosed with the high-risk type, which can develop a fatal phenotype that requires earlier diagnosis and personalized treatment [4]. Surgery and radiotherapy are the first choices for the treatment of localized PCa [5]. Radical prostatectomy contributes to reducing mortality and improving survival rates [6]. Currently, although multiple biomarkers have been identified to be linked to PCa pathogenesis and have been proposed for treatment [7], the clinical effects of these targets are © The Author(s) 2025. Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted b

FAQs

What is the main biological role of KAT3B proposed in the study?

KAT3B is proposed to function as a succinylase that mediates succinylation of c-Myc, thereby promoting its stability and contributing to PCa progression.

How did the study measure KAT3B and its cellular effects?

KAT3B expression was measured by qRT-PCR, Western blot, and immunofluorescence. Cellular viability, apoptosis, migration, and invasion were assessed using CCK-8, flow cytometry, and transwell assays.

What mechanism links KAT3B to c-Myc behavior in PCa cells?

KAT3B mediates the succinylation of c-Myc and promotes c-Myc stability. Restoring c-Myc expression reverses the suppressive effects of KAT3B downregulation.

Sep 29, 2026

Uploaded by Ben