Quantitative Proteomics Analysis Reveals Novel Insights into Mechanisms of Action of Long Noncoding RNA Hox Transcript Antisense Intergenic RNA (HOTAIR) in HeLa Cells*

Zheng, Peng; Xiong, Qian; Wu, Ying; Chen, Ying; Chen, Zhuo; Fleming, Joy; Ding, Guiguang; Bi, Lijun; Ge, Feng

doi:10.1074/mcp.m114.043984

Cited by 50 publications

(60 citation statements)

References 78 publications

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“…In muscle, H19 regulates glucose metabolism by acting as an upstream regulator of let-7 whose role in glucose metabolism has been established [25]. A role of HOTAIR in maintaining energy metabolism has been found in cancer cells [26]. In our previous work, we found that HOTAIR was involved in malignant transformation induced in cells by cigarette smoke extract [44].…”

Section: Discussionmentioning

confidence: 96%

“…To assess some common lncRNAs related to energy metabolism [25][26][27][28], and noting that MALAT1 is involved in arsenite-induced malignant transformation of liver cells [21], we determined the levels of these lncRNAs in L-02 cells exposed to 2 μM arsenite for 24 h. The levels of H19, HOTAIR, and MALAT1 were higher in cells exposed to arsenite than in normal cells; of the three lncRNAs, the differential expression of MALAT1 was highest (Fig. 3A).…”

Section: In L-02 Cells Arsenite Increases Levels Of Lncrnas and Hifsmentioning

confidence: 93%

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The lncRNA MALAT1, acting through HIF-1α stabilization, enhances arsenite-induced glycolysis in human hepatic L-02 cells

Luo

Liu

Ling

et al. 2016

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Accelerated glycolysis, a common process in tumor cells called the Warburg effect, is associated with various biological phenomena. However, the role of glycolysis induced by arsenite, a well-established human carcinogen, is unknown. Long non-coding RNAs (lncRNAs) act as regulators in various cancers, but how lncRNAs regulate glucose metabolism remains largely unexplored. We have found that, in human hepatic epithelial (L-02) cells, arsenite increases lactate production; glucose consumption; and expression of glycolysis-related genes, including HK-2, Eno-1, and Glut-4. In L-02 cells exposed to arsenite, the lncRNA, metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), and hypoxia inducible factors (HIFs)-α, the transcriptional regulators of cellular response to hypoxia, are over-expressed. In addition, HIF-1α, not HIF-2α, is involved in arsenite-induced glycolysis, and MALAT1 enhances arsenite-induced glycolysis. Although MALAT1 regulates HIF-α and promotes arsenite-induced glycolysis, MALAT1 promotes glycolysis through HIF-1α, not HIF-2α. Moreover, arsenite-increased MALAT1 enhances the disassociation of Von Hippel-Lindau (VHL) tumor suppressor from HIF-1α, alleviating VHL-mediated ubiquitination of HIF-1α, which causes accumulation of HIF-1α. In sum, these findings indicate that MALAT1, acting through HIF-1α stabilization, is a mediator that enhances glycolysis induced by arsenite. These results provide a link between the induction of lncRNAs and the glycolysis in cells exposed to arsenite, and thus establish a previously unknown mechanism for arsenite-induced hepatotoxicity.

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Section: Discussionmentioning

confidence: 96%

Section: In L-02 Cells Arsenite Increases Levels Of Lncrnas and Hifsmentioning

confidence: 93%

The lncRNA MALAT1, acting through HIF-1α stabilization, enhances arsenite-induced glycolysis in human hepatic L-02 cells

Luo

Liu

Ling

et al. 2016

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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“…HOTAIR is a scaffold for the PRC2 and LSD1 complexes affecting H3K27 methylation and H3K4 demethylation for epigenetic gene silencing promoting cancer metastasis . HOTAIR decreases oxidative phosphorylation (OXPHOS) complex III subunit VII (UQCRQ) protein expression, thus reducing OXPHOS efficiency and suggesting that HOTAIR is important for mitochondrial function in HeLa cells (Zheng, et al 2015).…”

Section: Examples Of Lncrnas Dysregulated In Endocrine-related Cancersmentioning

confidence: 99%

Non-coding RNAs: long non-coding RNAs and microRNAs in endocrine-related cancers

Klinge

2018

Endocrine-Related Cancer

100

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Abstract:The human genome is 'pervasively transcribed' leading to a complex array of noncoding RNAs (ncRNAs) that far outnumber coding mRNAs. ncRNAs have regulatory roles in transcription and post-transcriptional processes as well numerous cellular functions that remain to be fully described. Best characterized of the 'expanding universe' of ncRNAs are the ~ 22 nucleotide microRNAs (miRNAs) that base-pair to target mRNA's 3' untranslated region within the RNA-induced silencing complex (RISC) and block translation and may stimulate mRNA transcript degradation. Long non-coding RNAs (lncRNAs) are classified as >200 nucleotides in length, but range up to several kb and are heterogeneous in genomic origin and function.LncRNAs fold into structures that interact with DNA, RNA, and proteins to regulate chromatin dynamics, protein complex assembly, transcription, telomere biology, and splicing. Some lncRNAs act as sponges for miRNAs and decoys for proteins. Nuclear-encoded lncRNAs can be taken up by mitochondria and lncRNAs are transcribed from mtDNA. Both miRNAs and lncRNAs are dysregulated in endocrine cancers. This review provides an overview on the current understanding of the regulation and function of selected lncRNAs and miRNAs, and their interaction, in endocrine-related cancers: breast, prostate, endometrial, and thyroid.

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“…For example, studies showed that lncRNAs are dysregulated after EGCG treatment in lung cancer, nasopharyngeal carcinoma, prostatic hyperplasia, osteoarthritis, etc [33][34][35] However, whether lncRNAs mediated the protective role of catechin, a kind of bioactive polyphenol that has a variety of pharmacological and biological properties and plays a protective role in MI/R injury, 14 against H/R-induced myocardial cell apoptosis or MI/R injury is largely unknown. 40 Akt/Gsk-3β pathway has been shown to be involved in modulating oxidative stress and apoptosis, and the activation of Akt/Gsk-3β pathway preserved heart function and alleviated MI/R injury. 39 For example, lncRNA HOTAIR knockdown increased ROS production and caused mitochondrial swelling in HeLa cells, indicating lncRNA HOTAIR knockdown led to mitochondrial dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Catechin relieves hypoxia/reoxygenation‐induced myocardial cell apoptosis via down‐regulating lncRNA MIAT

Wei

et al. 2020

J Cellular Molecular Medi

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Background Catechin protects heart from myocardial ischaemia/reperfusion (MI/R) injury. However, whether catechin inhibits H/R‐induced myocardial cell apoptosis is largely unknown. Objective This study aims to investigate the underlying mechanism of catechin in inhibiting the apoptosis of H/R‐induced myocardial cells. Methods LncRNA MIAT expression was detected by qRT‐PCR. Cell viability of H9C2 cells was detected using CCK‐8 assay. The apoptosis of H9C2 cells was detected by flow cytometry. The interaction between CREB and MIAT promoter regions was confirmed by dual‐luciferase reporter gene assay and ChIP assay. Results In MI/R rats, catechin improved heart function and down‐regulated lncRNA MIAT expression in myocardial tissue. In H/R‐induced H9C2 cells, catechin protected against cell apoptosis, and lncRNA MIAT overexpression attenuated this protective effect of catechin. We confirmed that transcription factor CREB could bind to MIAT promoter region, and catechin suppressed lncRNA MIAT expression through up‐regulating CREB. Catechin improved mitochondrial function and relieved apoptosis through promoting Akt/Gsk‐3β activation. In addition, MIAT inhibited Akt/Gsk‐3β activation and promoted cell apoptosis in H/R‐induced H9C2 cells. Finally, we found catechin promoted Akt/Gsk‐3β activation through inhibiting MIAT expression in H/R‐induced H9C2 cells. Conclusion Catechin relieved H/R‐induced myocardial cell apoptosis through regulating CREB/lncRNA MIAT/Akt/Gsk‐3β pathway.

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Quantitative Proteomics Analysis Reveals Novel Insights into Mechanisms of Action of Long Noncoding RNA Hox Transcript Antisense Intergenic RNA (HOTAIR) in HeLa Cells*

Cited by 50 publications

References 78 publications

The lncRNA MALAT1, acting through HIF-1α stabilization, enhances arsenite-induced glycolysis in human hepatic L-02 cells

The lncRNA MALAT1, acting through HIF-1α stabilization, enhances arsenite-induced glycolysis in human hepatic L-02 cells

Non-coding RNAs: long non-coding RNAs and microRNAs in endocrine-related cancers

Catechin relieves hypoxia/reoxygenation‐induced myocardial cell apoptosis via down‐regulating lncRNA MIAT

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