糖酵解相关 lncRNA 在肿瘤进展中的调控功能:机制、事实和前景。

IF 5.3 2区 医学 Q1 PHARMACOLOGY & PHARMACY
Xinyi Peng , Shuhao Li , Anqi Zeng , Linjiang Song
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引用次数: 0

摘要

新陈代谢的改变是癌症的标志之一,而能量代谢的重编程(即 "沃伯格效应")与癌症的关系由来已久。癌细胞利用糖酵解过程迅速从葡萄糖、丙酮酸和乳酸中制造能量,这反过来又加速了癌症的生长,糖酵解也成为抗癌疗法的一个关键靶点。最近关于长非编码 RNA(lncRNA)的突破性发现为癌症发生机制揭开了新的篇章。人们普遍认为,lncRNA 通过糖酵解调节癌细胞的能量代谢。研究表明,LncRNAs 参与了多种癌症过程,如增殖、凋亡、迁移、侵袭和化疗抵抗,而糖酵解则会因 lncRNAs 的失调而增强或抑制。因此,癌症的生存和发展受到不同信号通路的影响。在这篇综述中,我们总结了 lncRNA 在多种癌症中的作用,并描述了它们在糖酵解中的作用机制。此外,我们还讨论了糖酵解和 lncRNA 在癌症治疗中的预测潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Regulatory function of glycolysis-related lncRNAs in tumor progression: Mechanism, facts, and perspectives

Regulatory function of glycolysis-related lncRNAs in tumor progression: Mechanism, facts, and perspectives

Altered metabolism is a hallmark of cancer, and reprogramming of energy metabolism, known as the “Warburg effect”, has long been associated with cancer. Cancer cells use the process of glycolysis to quickly manufacture energy from glucose, pyruvic acid, and lactate, which in turn accelerates the growth of cancer and glycolysis becomes a key target for anti-cancer therapies. Recent groundbreaking discoveries regarding long noncoding RNAs (lncRNAs) have opened a new chapter in the mechanism of cancer occurrence. It is widely recognized that lncRNAs regulate energy metabolism through glycolysis in cancer cells. LncRNAs have been demonstrated to engage in several cancer processes such as proliferation, apoptosis, migration, invasion, and chemoresistance, whereas glycolysis is enhanced or inhibited by the dysregulation of lncRNAs. As a result, cancer survival and development are influenced by different signaling pathways. In this review, we summarize the roles of lncRNAs in a variety of cancers and describe the mechanisms underlying their role in glycolysis. Additionally, the predictive potential of glycolysis and lncRNAs in cancer therapy is discussed.

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来源期刊
Biochemical pharmacology
Biochemical pharmacology 医学-药学
CiteScore
10.30
自引率
1.70%
发文量
420
审稿时长
17 days
期刊介绍: Biochemical Pharmacology publishes original research findings, Commentaries and review articles related to the elucidation of cellular and tissue function(s) at the biochemical and molecular levels, the modification of cellular phenotype(s) by genetic, transcriptional/translational or drug/compound-induced modifications, as well as the pharmacodynamics and pharmacokinetics of xenobiotics and drugs, the latter including both small molecules and biologics. The journal''s target audience includes scientists engaged in the identification and study of the mechanisms of action of xenobiotics, biologics and drugs and in the drug discovery and development process. All areas of cellular biology and cellular, tissue/organ and whole animal pharmacology fall within the scope of the journal. Drug classes covered include anti-infectives, anti-inflammatory agents, chemotherapeutics, cardiovascular, endocrinological, immunological, metabolic, neurological and psychiatric drugs, as well as research on drug metabolism and kinetics. While medicinal chemistry is a topic of complimentary interest, manuscripts in this area must contain sufficient biological data to characterize pharmacologically the compounds reported. Submissions describing work focused predominately on chemical synthesis and molecular modeling will not be considered for review. While particular emphasis is placed on reporting the results of molecular and biochemical studies, research involving the use of tissue and animal models of human pathophysiology and toxicology is of interest to the extent that it helps define drug mechanisms of action, safety and efficacy.
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