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长非编码 RNA 与 RNA 结合蛋白相互作用影响肿瘤糖代谢重编程的研究进展(综述)。

Research progress on the interaction between long non‑coding RNAs and RNA‑binding proteins to influence the reprogramming of tumor glucose metabolism (Review).

机构信息

Department of General Surgery, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou 563000, P.R. China.

出版信息

Oncol Rep. 2022 Sep;48(3). doi: 10.3892/or.2022.8365. Epub 2022 Jul 20.

DOI:10.3892/or.2022.8365
PMID:35856447
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9350995/
Abstract

As epigenetic regulators, long non‑coding RNAs (lncRNAs) are involved in various important regulatory processes and typically interact with RNA‑binding proteins (RBPs) to exert their core functional effects. An increasing number of studies have demonstrated that lncRNAs can regulate the occurrence and development of cancer through a variety of complex mechanisms and can also participate in tumor glucose metabolism by directly or indirectly regulating the Warburg effect. As one of the metabolic characteristics of tumor cells, the Warburg effect provides a large amount of energy and numerous intermediate products to meet the consumption demands of tumor metabolism, providing advantages for the occurrence and development of tumors. The present review article summarizes the regulatory effects of lncRNAs on the reprogramming of glucose metabolism after interacting with RBPs in tumors. The findings discussed herein may aid in the better understanding of the pathogenesis of malignancies, and may provide novel therapeutic targets, as well as new diagnostic and prognostic markers for human cancers.

摘要

作为表观遗传调控因子,长链非编码 RNA(lncRNA)参与各种重要的调控过程,通常与 RNA 结合蛋白(RBP)相互作用以发挥其核心功能效应。越来越多的研究表明,lncRNA 可以通过多种复杂机制调节癌症的发生和发展,并且还可以通过直接或间接调节瓦伯格效应参与肿瘤葡萄糖代谢。作为肿瘤细胞的代谢特征之一,瓦伯格效应提供大量能量和许多中间产物,以满足肿瘤代谢的消耗需求,为肿瘤的发生和发展提供了优势。本文综述了 lncRNA 通过与肿瘤中的 RBPs 相互作用对葡萄糖代谢重编程的调控作用。本文讨论的研究结果可能有助于更好地理解恶性肿瘤的发病机制,并为人类癌症提供新的治疗靶点以及新的诊断和预后标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db4b/9350995/0010bea4e5e5/or-48-03-08365-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db4b/9350995/e48c42f4cc2d/or-48-03-08365-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db4b/9350995/0010bea4e5e5/or-48-03-08365-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db4b/9350995/e48c42f4cc2d/or-48-03-08365-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db4b/9350995/0010bea4e5e5/or-48-03-08365-g01.jpg

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LNCAROD enhances hepatocellular carcinoma malignancy by activating glycolysis through induction of pyruvate kinase isoform PKM2.
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lncRNA GAS6-AS1 inhibits progression and glucose metabolism reprogramming in LUAD via repressing E2F1-mediated transcription of GLUT1.长链非编码RNA GAS6-AS1通过抑制E2F1介导的葡萄糖转运蛋白1(GLUT1)转录来抑制肺腺癌的进展和糖代谢重编程。
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