Yan-Wen Wang , Ti Chu , Xue-Li Wang , Yong-Qi Fan , Lei Cao , Yu-Hang Chen , Yi-Wen Zhu , Hong-Xia Liu , Xin-Ying Ji , Dong-Dong Wu
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引用次数: 0
Abstract
Cystathionine β-synthase (CBS) occupies a key position as the initiating and rate-limiting enzyme in the sulfur transfer pathway and plays a vital role in health and disease. CBS is responsible for regulating the metabolism of cysteine, the precursor of glutathione (GSH), an important antioxidant in the body. Additionally, CBS is one of the three enzymes that produce hydrogen sulfide (H2S) in mammals through a variety of mechanisms. The dysregulation of CBS expression in cancer cells affects H2S production through direct or indirect pathways, thereby influencing cancer growth and metastasis by inducing angiogenesis, facilitating proliferation, migration, and invasion, modulating cellular energy metabolism, promoting cell cycle progression, and inhibiting apoptosis. It is noteworthy that CBS expression exhibits complex changes in different cancer models. In this paper, we focus on the CBS synthesis and metabolism, tissue distribution, potential mechanisms influencing tumor growth, and relevant signaling pathways. We also discuss the impact of pharmacological CBS inhibitors and silencing CBS in preclinical cancer models, supporting their potential as targeted cancer therapies.
胱硫醚β-合成酶(CBS)作为硫转移途径中的起始酶和限速酶,在健康和疾病中发挥着关键作用。CBS 负责调节半胱氨酸的代谢,半胱氨酸是谷胱甘肽(GSH)的前体,而谷胱甘肽是人体重要的抗氧化剂。此外,CBS 还是哺乳动物体内通过多种机制产生硫化氢(H2S)的三种酶之一。癌细胞中 CBS 的表达失调会通过直接或间接途径影响 H2S 的产生,从而通过诱导血管生成、促进增殖、迁移和侵袭、调节细胞能量代谢、促进细胞周期进展和抑制细胞凋亡等方式影响癌症的生长和转移。值得注意的是,CBS 的表达在不同癌症模型中表现出复杂的变化。本文重点探讨了 CBS 的合成与代谢、组织分布、影响肿瘤生长的潜在机制以及相关信号通路。我们还讨论了药理 CBS 抑制剂和沉默 CBS 对临床前癌症模型的影响,支持它们作为癌症靶向疗法的潜力。
期刊介绍:
Cellular Signalling publishes original research describing fundamental and clinical findings on the mechanisms, actions and structural components of cellular signalling systems in vitro and in vivo.
Cellular Signalling aims at full length research papers defining signalling systems ranging from microorganisms to cells, tissues and higher organisms.