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LncRNA 相关 PKM2 在癌症代谢中的分子机制。

The molecular mechanisms of LncRNA-correlated PKM2 in cancer metabolism.

机构信息

Department of Pharmacy, YueYang Maternal-Child Medicine Health Hospital, Yueyang 414000, Hunan, China.

Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province, School of Medicine, Hunan Normal University, Changsha 410013, Hunan, China.

出版信息

Biosci Rep. 2019 Nov 29;39(11). doi: 10.1042/BSR20192453.

DOI:10.1042/BSR20192453
PMID:31654067
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6851521/
Abstract

Reprogrammed metabolism is an important hallmark of cancer cells. Pyruvate kinase (PK) is one of the major rate-limiting enzymes in glucose metabolism. The M2 isoform of PK (PKM2), is considered to be an important marker of metabolic reprogramming and one of the key enzymes. Recently, through the continuous development of genome-wide analysis and functional studies, accumulating evidence has demonstrated that long non-coding RNAs (LncRNAs) play vital regulatory roles in cancer progression by acting as either potential oncogenes or tumor suppressors. Furthermore, several studies have shown that up-regulation of PKM2 in cancer tissues is associated with LncRNAs expression and patient survival. Thus, scientists have begun to unveil the mechanism of LncRNA-associated PKM2 in cancer metabolic progression. Based on these novel findings, in this mini-review, we summarize the detailed molecular mechanisms of LncRNA related to PKM2 in cancer metabolism. We expect that this work will promote a better understanding of the molecular mechanisms of PKM2, and provide a profound potential for targeting PKM2 to treat tumors.

摘要

代谢重编程是癌细胞的一个重要标志。丙酮酸激酶(PK)是糖代谢中的主要限速酶之一。PK 的 M2 同工酶(PKM2)被认为是代谢重编程的重要标志物之一,也是关键酶之一。最近,通过全基因组分析和功能研究的不断发展,越来越多的证据表明,长链非编码 RNA(lncRNA)通过作为潜在的癌基因或肿瘤抑制因子,在癌症进展中发挥重要的调节作用。此外,一些研究表明,癌症组织中 PKM2 的上调与 lncRNA 的表达和患者的生存有关。因此,科学家们开始揭示 lncRNA 与 PKM2 在癌症代谢进展中的相关机制。基于这些新发现,在这篇综述中,我们总结了 lncRNA 与 PKM2 相关的癌症代谢的详细分子机制。我们期望这项工作将促进对 PKM2 分子机制的更好理解,并为靶向 PKM2 治疗肿瘤提供更深入的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f38c/6851521/373abf4d6a82/bsr-39-bsr20192453-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f38c/6851521/cc4ea09149c4/bsr-39-bsr20192453-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f38c/6851521/34d5f29e4967/bsr-39-bsr20192453-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f38c/6851521/373abf4d6a82/bsr-39-bsr20192453-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f38c/6851521/cc4ea09149c4/bsr-39-bsr20192453-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f38c/6851521/34d5f29e4967/bsr-39-bsr20192453-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f38c/6851521/373abf4d6a82/bsr-39-bsr20192453-g3.jpg

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Biomed Pharmacother. 2019 Sep;117:109069. doi: 10.1016/j.biopha.2019.109069. Epub 2019 Jun 7.
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PKM2 Knockdown Induces Autophagic Cell Death via AKT/mTOR Pathway in Human Prostate Cancer Cells.
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