LncRNA EPB41L4A-AS1 regulates glycolysis and glutaminolysis by mediating nucleolar translocation of HDAC2

Liao, Meijian; Liao, Weijie; Xu, Ning; Li, Bing; Liu, Fuhai; Zhang, Shikuan; Wang, Yanzhi; Wang, Songmao; Zhu, Yuanchang; Chen, Deheng; Xie, Weidong; Jiang, Yuyang; Cao, Liu; Yang, Burton B.; Zhang, Yaou

doi:10.1016/j.ebiom.2019.01.035

Cited by 126 publications

(123 citation statements)

References 56 publications

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“…Knockdown of TIGA1 promotes microtubule depolymerization via reduced acetylated α-tubulin, which induces cellular stress and ROS production due to VDAC block by binding with free tubulin. Consequently, p38 is phosphorylated and subsequently increases HIF-1α level [101].…”

Section: Lncrnas Regulate Glutamine Metabolismmentioning

confidence: 99%

LncRNAs regulate metabolism in cancer

et al. 2020

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Metabolic reprogramming is a hallmark of cancer. Mammalian genome is characterized by pervasive transcription, generating abundant non-coding RNAs (ncRNAs). Long non-coding RNAs (lncRNAs) are freshly discovered functional ncRNAs exerting extensive regulatory impact through diverse mechanisms. Emerging studies have revealed widespread roles of lncRNAs in the regulation of various cellular activities, including metabolic pathways. In this review, we summarize the latest advances regarding the regulatory roles of lncRNAs in cancer metabolism, particularly their roles in mitochondrial function, glucose, glutamine, and lipid metabolism. Moreover, we discuss the clinical application and challenges of targeting lncRNAs in cancer metabolism. Understanding the complex and special behavior of lncRNAs will allow a better depiction of cancer metabolic networks and permit the development of lncRNA-based clinical therapies by targeting cancer metabolism.

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Section: Lncrnas Regulate Glutamine Metabolismmentioning

confidence: 99%

LncRNAs regulate metabolism in cancer

et al. 2020

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“…Long non-coding RNAs (lncRNAs), a set of non-coding RNAs (ncRNAs) with a length of more than 200 nucleotides, make a significant contribution in cancer biology and serve as biomarkers and therapeutic targets for many human neoplastic diseases [6][7][8]. In recent years, the aberrant expression of lncRNAs has been discovered in various types of tumours, acting as oncogenes or tumour suppressors [9][10][11]. Two molecular mechanisms of lncRNAs in the development of glioma have been proposed.…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA SNHG5 promotes glioma progression via miR-205/E2F3 axis

Liu

Luo

et al. 2019

Bioscience Reports

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In recent years, many studies have reported on the abnormal expression and correlation of long non-coding RNAs (lncRNAs) in tumours. However, the accurate molecular mechanism of lncRNAs in glioma is still in its infancy. In the present study, we aimed to explore the molecular mechanism of small nucleolar RNA host gene 5 (SNHG5) in glioma progression. First, we found that SNHG5 expression was higher in glioma and was related to glioma glucose uptake, migration and invasion. Second, through a series of assays, we concluded that SNHG5 acts as a sponge for miR-205, which inhibits tumour growth in glioma by targeting E2F transcription factor 3 (E2F3). Third, using a xenograft mouse model, we demonstrated that SNHG5 regulates tumourigenesis in vivo. Taken together, our results show that the SNHG5/miR-205/E2F3 axis is involved in glioma progression and may provide a new therapeutic target for the diagnosis and therapy of glioma.

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“…Interestingly, reactive oxygen species were augmented, inducing the transcriptional activation of P-eIF2α/ATF4; as a consequence, the overexpression of the SNAT5 (SN2) transporter was induced, leading to an increase in glutamine consumption. Moreover, it was also demonstrated that the absence of EPB41L4A-AS1 upregulates glutaminolysis-related members such as ASCT2, GLS, ME1 and ME2 [126] (Figure 3). catabolism, which depends on GLS, although the implicated mechanisms remain unknown [127] ( Figure 3).…”

Section: Lncrna Epb41l4a-as1mentioning

confidence: 94%

Non-Coding RNAs as Key Regulators of Glutaminolysis in Cancer

Ortiz-Pedraza

Muñoz-Bello

Olmedo-Nieva

et al. 2020

IJMS

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Cancer cells exhibit exacerbated metabolic activity to maintain their accelerated proliferation and microenvironmental adaptation in order to survive under nutrient-deficient conditions. Tumors display an increase in glycolysis, glutaminolysis and fatty acid biosynthesis, which provide their energy source. Glutamine is critical for fundamental cellular processes, where intermediate metabolites produced through glutaminolysis are necessary for the maintenance of mitochondrial metabolism. These include antioxidants to remove reactive oxygen species, and the generation of the nonessential amino acids, purines, pyrimidines and fatty acids required for cellular replication and the activation of cell signaling. Some cancer cells are highly dependent on glutamine consumption since its catabolism provides an anaplerotic pathway to feed the Krebs cycle. Intermediate members of the glutaminolysis pathway have been found to be deregulated in several types of cancers and have been proposed as therapeutic targets and prognostic biomarkers. This review summarizes the main players in the glutaminolysis pathway, how they have been found to be deregulated in cancer and their implications for cancer maintenance. Furthermore, non-coding RNAs are now recognized as new participants in the regulation of glutaminolysis; therefore, their involvement in glutamine metabolism in cancer is discussed in detail.Int. J. Mol. Sci. 2020, 21, 2872 2 of 26 an increased glucose consumption in relation to normal differentiated tissues. Now we know that glutamine metabolism is as important as glucose metabolism for the production of macromolecules in cancer [1].Glutamine is an abundant amino acid involved in energy production, homeostasis in pro/antioxidant species and the activation of signaling pathways in cancer. In addition to the antioxidant glutathione (GSH), nucleotides, lipids and amino acids are formed from glutamine metabolism. All of these are needed for many metabolic functions such as growth, proliferation, cell survival and defense against oxidative stress [2]. Glutamine contributes, with reduced nitrogen, to the de novo biosynthesis of diverse nitrogen-containing compounds, such as purine and pyrimidine nucleotides, glucosamine-6-phosphate and nonessential amino acids.As glutamine is the most abundant amino acid in the blood and muscle tissue, normal proliferating cells use glutamine metabolism as an energy source, mediated by its catabolic products, glutamate and α-ketoglutarate (α-kG), the latter being an intermediate of the tricarboxylic acid cycle (TCA) or Krebs cycle [3]. In 1950, Harry Eagle observed that HeLa tumor cells require an excess of glutamine, in relation to other amino acids in the culture medium, for optimal growth. Furthermore, it has been reported that tumors consume glutamine faster than the surrounding normal tissue [4]. Moreover, most cancer cells are dependent on glutamine being unable to survive under glutamine starvation, an effect that has been termed glutamine addiction [5]. Various types of cancers are high...

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LncRNA EPB41L4A-AS1 regulates glycolysis and glutaminolysis by mediating nucleolar translocation of HDAC2

Cited by 126 publications

References 56 publications

LncRNAs regulate metabolism in cancer

LncRNAs regulate metabolism in cancer

Long non-coding RNA SNHG5 promotes glioma progression via miR-205/E2F3 axis

Non-Coding RNAs as Key Regulators of Glutaminolysis in Cancer

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