期刊
MOLECULAR BIOLOGY REPORTS
卷 48, 期 3, 页码 2713-2727出版社
SPRINGER
DOI: 10.1007/s11033-021-06247-7
关键词
Long non-coding RNA; Warburg effect; Glucose metabolism; Small molecular inhibitors; RNA inference; Antisense oligonucleotide
Metabolism reprogramming, especially glucose metabolism, is a hallmark of cancer cells that promotes proliferation, metastasis, and drug resistance. Protein-coding genes play a role in this process, and long non-coding RNA shows potential as a significant regulator in glycolysis-targeted cancer therapy.
Metabolism reprogramming is one of the hallmarks of cancer cells, especially glucose metabolism, to promote their proliferation, metastasis and drug resistance. Cancer cells tend to depend on glycolysis for glucose utilization rather than oxidative phosphorylation, which is called the Warburg effect. Genome instability of oncogenes and tumor-inhibiting factors is the culprits for this anomalous glycolytic fueling, which results in dysregulating metabolism-related enzymes and metabolic signaling pathways. It has been extensively demonstrated that protein-coding genes are involved in this process; therefore, glycolysis-targeted therapy has been widely used in anti-tumor combined therapy via small molecular inhibitors of key enzymes and regulatory molecular. The long non-coding RNA, which is a large class of regulatory RNA with longer than 200 nucleotides, is the novel and significant regulator of various biological processes, including metabolic reprogramming. RNA interference and synthetic antisense oligonucleotide for RNA reduction have developed rapidly these years, which presents potent anti-tumor effects both in vitro and in vivo. However, lncRNA-based glycolysis-targeted cancer therapy, as the highly specific and less toxic approach, is still under the preclinical phase. In this review, we highlight the role of lncRNA in glucose metabolism and dissect the feasibility and limitations of this clinical development, which may provide potential targets for cancer therapy.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据