The mechanism of PFK-1 in the occurrence and development of bladder cancer by regulating ZEB1 lactylation

Sep 21, 2026

Uploaded by Finn

Bladder cancer is a frequent genitourinary malignancy, driven by altered metabolism and transcriptional regulation. This study investigates how phosphofructokinase 1 (PFK-1) influences bladder cancer development through ZEB1 lactylation. Experimental work assesses cell viability, glucose utilization, lactate production, and gene expression by qRT-PCR. Results show elevated ZEB1 in bladder cancer, and PFK-1 disruption reduces glycolysis, proliferation, migration, invasion, and tumor growth, partly by limiting histone lactylation and ZEB1 transcriptional activity.

LanguageEnglish

CategoryResearch & Report

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Pages10

Reading Time25 min

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Abstract

Background

Methods

Results

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Introduction

Wang et al. BMC Urology (2024) 24:59 [https://doi.org/10.1186/s12894-024-01444-5](https://doi.org/10.1186/s12894-024-01444-5) BMC Urology RESEARCH Open Access The mechanism of PFK-1 in the occurrence and development of bladder cancer by regulating ZEB1 lactylation Rong Wang 1*, Fei Xu 1, Zhengjia Yang 1, Jian Cao 1, Liqi Hu 1 and Yangyang She 1 Abstract Background Bladder cancer (BC) is one of the most common malignancies of the genitourinary system. Phosphofructokinase 1 (PFK-1) is one of member of PFK, which plays an important role in reprogramming cancer metabolism, such as lactylation modification. Zinc finger E-box-binding homeobox 1 (ZEB1) has been demonstrated to be a oncogene in many cancers. Therefore, this study was performed to explore the effects of PFK-1 on the lactylation of ZEB1 in BC development. Methods Cell viability was measured using the CCK-8 kit. The glucose assay kit and lactate assay kit were used to detect glucose utilization and lactate production. The DNA was purified and quantified by qRT-PCR. Results In the present study, we found that ZEB1 expression levels were significantly elevated in bladder cancer cells. Impaired PFK-1 expression inhibits proliferation, migration, and invasion of BC cells and suppresses tumour growth in vivo. We subsequently found that knockdown of PFK-1 decreases glycolysis, including reduced glucose consumption, lactate production and total extracellular acidification rate (ECAR) . Mechanistically, PFK-1 inhibits histone lactylation of bladder cancer cells, and thus inhibits the transcription activity of ZEB1 . Conclusion Our results suggest that PFK-1 can inhibit the malignant phenotype of bladder cancer cells by mediating the lactylation of ZEB1 . These findings suggested PFK-1 to be a new potential target for bladder cancer therapy. Keywords Bladder cancer, PFK-1, ZEB1, Lactylation, Glycolysis Introduction Bladder cancer (BC) is one of the most common malignancies ofthe genitourinary system [1]. With the increasing incidence and mortality, bladder cancer causes more than 170,000 deaths each year. When it invades the muscle, BC develops into two distinct sub-types: non-muscle invasive BC (75%) and muscle invasive BC (25%), with *Correspondence: RongWang [drwangr@163.com](drwangr@163.com) 1Department of Urology, Hangzhou Linping TCM Hospital, No.101 Yuncheng Street, Tangxi Town, Linping District, Hangzhou City 311106, China muscle invasive BC having a higher risk of metastasis. Despite significant advances in clinical treatments such as surgery, chemotherapy and radiotherapy over the past decades, the 5-year survival rate for patients with BC remains low [2]. Lymph node metastasis is considered to be the main route of metastasis and the main cause of poor prognosis in BC, with the 5-year survival rate of patients decreasing from 77.6 to 18.6%[3]. Lack of early diagnosis and effective treatment leads to poor clinical regression in BC patients, thus, it is essential to explore novel molecular mechanisms and therapeutic targets for BC [4]. © The Author(s) 2024. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, 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 changes were made. 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 by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit [http://creativecommons.org/l](http://creativecommons.org/l)icenses/by/4.0/. The Creative Common

FAQs

What is the main focus of this study on bladder cancer?

The study examines how PFK-1 regulates ZEB1 lactylation and how this affects bladder cancer occurrence and development.

How was glycolysis and lactate metabolism evaluated?

Glucose utilization and lactate production were measured using glucose and lactate assay kits, with DNA expression quantified by qRT-PCR.

What effect does impairing PFK-1 have on bladder cancer cells and tumors?

Impaired PFK-1 expression inhibits proliferation, migration, and invasion of bladder cancer cells and suppresses tumor growth in vivo while reducing glycolysis-related outputs.

Sep 21, 2026

Uploaded by Finn