Jiang Zhengyan, Gu Zhengrong, Lu Xianyan, Wen Wei
Digestive Department, Jiangsu Second Chinese Medicine Hospital, Nanjing, China.
Digestive Department, Suzhou Wujiang District Hospital of Traditional Chinese Medicine (Suzhou Wujiang District Second People's Hospital), Suzhou, China.
Transl Cancer Res. 2024 Jul 31;13(7):3854-3868. doi: 10.21037/tcr-23-2244. Epub 2024 Jul 22.
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.
该综述深入探讨了代谢失调与胃癌（GC）发生发展之间的复杂相互作用，揭示了这种常见恶性肿瘤的一个关键方面。GC是全球癌症相关死亡的主要原因之一，其发展轨迹受多种因素影响，其中代谢失调和异常基因表达起着重要作用。本文阐述了代谢失调在GC发生过程中的基本作用，揭示了异常糖酵解现象，如以瓦伯格效应为代表的现象，以及脂质和氨基酸代谢异常。它描述了这些紊乱如何推动癌症进程，促进细胞不受控制地增殖和存活。此外，还阐明了代谢与GC细胞活力之间的复杂联系，强调了代谢重编程对肿瘤能量动态和代谢副产物积累的深远影响，而这些副产物进一步促进了恶性生长。综述的一个关键部分是探索与GC发病机制相关的关键代谢相关基因。其中，MYC和TP53备受关注，阐述了它们通过调节代谢途径在驱动肿瘤发生中的关键作用。这些基因途径是协调GC发展的复杂网络中的关键节点，为治疗干预提供了有价值的靶点。本综述展望未来，描绘了基于对GC代谢失调的认识而产生的潜在治疗途径。它强调了针对肿瘤进展中特定代谢途径的靶向治疗的前景，以及利用代谢和传统抗癌方式的联合治疗策略的新兴潜力。本质上，这篇全面的综述就像一座灯塔，照亮了GC发病机制中代谢失调的复杂图景。通过对代谢异常及其遗传基础的细致探索，它不仅丰富了我们对GC生物学的理解，还揭示了有望彻底改变其临床管理的新治疗前景。
