The Role of Dysregulated Metabolism and Associated Genes in Gastric Cancer Initiation and Development

Sep 21, 2026

Uploaded by Liam

The review examines how metabolic dysregulation and related gene alterations drive gastric cancer (GC) initiation and progression. GC is a major cause of cancer death worldwide, with diverse influences in which aberrant metabolism and abnormal gene expression play key roles. The article highlights disruptions such as Warburg-like glycolysis and disturbed lipid and amino-acid metabolism, linking them to uncontrolled proliferation, survival, and tumor energy remodeling. It further surveys key metabolic genes including MYC and TP53 as actionable nodes for therapeutic targeting, and discusses prospects for targeted and combination therapies.

LanguageEnglish

CategoryResearch & Report

FormatPDF

Pages15

Reading Time38 min

AccessFree to download

Introduction

Gastric cancer burden and risk factors

Metabolic dysregulation as a cancer hallmark

Metabolic disorders in GC development, treatment, and prognosis

Review of metabolic pathways and genetic drivers

Glycolysis abnormalities and the Warburg effect

Lipid and amino-acid metabolism anomalies

Metabolism–cell survival and energy remodeling

Key metabolic-related genes in GC (MYC, TP53)

Therapeutic implications and future directions

The role of dysregulated metabolism and associated genes in gastric cancer initiation and development Zhengyan Jiang1\#, Zhengrong Gu1\#, Xianyan Lu2, Wei Wen1 1Digestive Department, Jiangsu Second Chinese Medicine Hospital, Nanjing, China; 2Digestive Department, Suzhou Wujiang District Hospital of Traditional Chinese Medicine (Suzhou Wujiang District Second People’s Hospital), Suzhou, China Contributions: (I) Conception and design: X Lu, W Wen, Z Jiang; (II) Administrative support: X Lu; (III) Provision of study materials or patients: Z Jiang; (IV) Collection and assembly of data: Z Jiang; (V) Data analysis and interpretation: Z Jiang, Z Gu; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors. \#These authors contributed equally to this work. Correspondence to: Wei Wen, MD. Digestive Department, Jiangsu Second Chinese Medicine Hospital, No. 23 Nanhu Road, Nanjing 210002, China. Email: [13776692809@163.com](13776692809@163.com); Xianyan Lu, MD. Digestive Department, Suzhou Wujiang District Hospital of Traditional Chinese Medicine (Suzhou Wujiang District Second People’s Hospital), No. 999 Dachun Road, Suzhou 215000, China. Email: [624584870@qq.com](624584870@qq.com). Abstract: The review delves into the intricate interplay between metabolic dysregulation and the onset and progression of gastric cancer (GC), shedding light on a pivotal aspect of this prevalent malignancy. GC stands as one of the leading causes of cancer-related mortality worldwide, its trajectory influenced by a multitude of factors, among which metabolic dysregulation and aberrant gene expression play significant roles. The article navigates through the fundamental roles of metabolic dysregulation in the genesis of GC, unveiling phenomena such as aberrant glycolysis, epitomized by the Warburg effect, alongside anomalies in lipid and amino acid metabolism. It delineates how these disruptions fuel the cancerous process, facilitating uncontrolled cell proliferation and survival. Furthermore, the intricate nexus between metabolism and the vitality of GC cells is elucidated, underscoring the profound influence of metabolic reprogramming on tumor energy dynamics and the accrual of metabolic by-products, which further perpetuate malignant growth. A pivotal segment of the review entails an exploration of key metabolic-related genes implicated in GC pathogenesis. MYC and TP53 are spotlighted among others, delineating their pivotal roles in driving tumorigenesis through metabolic pathway modulation. These genetic pathways serve as critical nodes in the intricate network orchestrating GC development, providing valuable targets for therapeutic intervention. This review embarks on a forward-looking trajectory, delineating the potential therapeutic avenues stemming from insights into metabolic dysregulation in GC. It underscores the promise of targeted therapies directed towards specific metabolic pathways implicated in tumor progression, alongside the burgeoning potential of combination therapy strategies leveraging both metabolic and conventional anti-cancer modalities. In essence, this comprehensive review serves as a beacon, illuminating the intricate landscape of metabolic dysregulation in GC pathogenesis. Through its nuanced exploration of metabolic aberrations and their genetic underpinnings, it not only enriches our understanding of GC biology but also unveils novel therapeutic vistas poised to revolutionize its clinical management. Keywords: Genes; metabolism; gastric cancer (GC) Submitted Dec 06, 2023. Accepted for publication Jun 04, 2024. Published online Jul 22, 2024. doi: 10.21037/tcr-23-2244 View this article at: [https://dx.doi.org/10.21037/tcr-23-2244](https://dx.doi.org/10.21037/tcr-23-2244) © Translational Cancer Research. All rights reserved. Transl Cancer Res 2024;13(7):3854-3868 | [https://dx.doi.org/10.21037/tcr-23-2244](https://dx.doi.org/10.21037/tcr-23-2244) Translational Cancer Resear

FAQs

What metabolic disruptions are emphasized in gastric cancer?

The review highlights aberrant glycolysis, epitomized by the Warburg effect, and abnormalities in lipid and amino-acid metabolism.

How do metabolic dysregulation and gene expression contribute to GC progression?

Metabolic disruptions fuel cancerous processes by supporting uncontrolled cell proliferation and survival, while metabolic reprogramming reshapes tumor energy dynamics and accumulation of metabolic by-products. It also links these effects to dysregulated gene networks.

Which genes are spotlighted as key metabolic-related drivers in GC?

MYC and TP53 are specifically spotlighted among others for their pivotal roles in driving tumorigenesis through modulation of metabolic pathways.

Sep 21, 2026

Uploaded by Liam