scholarly journals Resveratrol, MicroRNAs, Inflammation, and Cancer

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Esmerina Tili ◽  
Jean-Jacques Michaille
Keyword(s):  
Tumor Suppressor ◽  
Inflammatory Response ◽  
Target Genes ◽  
Human Cancer ◽  
Noncoding Rnas ◽  
Preclinical Studies ◽  
Anticancer Properties ◽  
Natural Polyphenol ◽  
The Status ◽  
Anti Inflammatory

MicroRNAs are short noncoding RNAs that regulate the expression of many target genes posttranscriptionally and are thus implicated in a wide array of cellular and developmental processes. The expression ofmiR-155ormiR-21is upregulated during the course of the inflammatory response, but these microRNAs are also considered oncogenes due to their upregulation of expression in several types of tumors. Furthermore, it is now well established that inflammation is associated with the induction or the aggravation of nearly 25% of cancers. Therefore, the above microRNAs are thought to link inflammation and cancer. Recently, resveratrol (trans-3,4′,5-trihydroxystilbene), a natural polyphenol with antioxidant, anti-inflammatory, and anticancer properties, currently at the stage of preclinical studies for human cancer prevention, has been shown to induce the expression ofmiR-663, a tumor-suppressor and anti-inflammatory microRNA, while downregulatingmiR-155andmiR-21. In this paper we will discuss how the use of resveratrol in therapeutics may benefit from the preanalyses on the status of expression ofmiR-155ormiR-21as well as ofTGFβ1. In addition, we will discuss how resveratrol activity might possibly be enhanced by simultaneously manipulating the levels of its key target microRNAs, such asmiR-663.

Role of VHL Gene Mutation in Human Cancer

2004 ◽  
Vol 22 (24) ◽  
pp. 4991-5004 ◽  
Author(s):  
William Y. Kim ◽  
William G. Kaelin
Keyword(s):  
Tumor Suppressor ◽  
Target Genes ◽  
Human Cancer ◽  
Critical Role ◽  
Hypoxia Inducible Factor ◽  
Suppressor Gene ◽  
Tumor Formation ◽  
Hereditary Cancer Syndrome ◽  
Cancer Syndrome ◽  
Von Hippel Lindau

Germline inactivation of the von Hippel-Lindau (VHL) tumor suppressor gene causes the von Hippel-Lindau hereditary cancer syndrome, and somatic mutations of this gene have been linked to the development of sporadic hemangioblastomas and clear-cell renal carcinomas. The VHL tumor suppressor protein (pVHL), through its oxygen-dependent polyubiquitylation of hypoxia-inducible factor (HIF), plays a central role in the mammalian oxygen-sensing pathway. This interaction between pVHL and HIF is governed by post-translational prolyl hydroxylation of HIF in the presence of oxygen by a conserved family of Egl-nine (EGLN) enzymes. In the absence of pVHL, HIF becomes stabilized and is free to induce the expression of its target genes, many of which are important in regulating angiogenesis, cell growth, or cell survival. Moreover, preliminary data indicate that HIF plays a critical role in pVHL-defective tumor formation, raising the possibility that drugs directed against HIF or its downstream targets (such as vascular endothelial growth factor) might one day play a role in the treatment of hemangioblastoma and renal cell carcinoma. On the other hand, clear genotype-phenotype correlations are emerging in VHL disease and can be rationalized if pVHL has functions separate from its control of HIF.

scholarly journals Inferring and analyzing module-specific lncRNA–mRNA causal regulatory networks in human cancer

2018 ◽  
Vol 20 (4) ◽  
pp. 1403-1419 ◽  
Author(s):  
Junpeng Zhang ◽  
Thuc Duy Le ◽  
Lin Liu ◽  
Jiuyong Li
Keyword(s):  
Gene Expression ◽  
Regulatory Networks ◽  
Target Genes ◽  
Human Cancer ◽  
Noncoding Rnas ◽  
Lung Squamous Cell Carcinoma ◽  
Third Party ◽  
Biological Functions ◽  
Complementary Method ◽  
Statistical Correlations

Abstract It is known that noncoding RNAs (ncRNAs) cover ∼98% of the transcriptome, but do not encode proteins. Among ncRNAs, long noncoding RNAs (lncRNAs) are a large and diverse class of RNA molecules, and are thought to be a gold mine of potential oncogenes, anti-oncogenes and new biomarkers. Although only a minority of lncRNAs is functionally characterized, it is clear that they are important regulators to modulate gene expression and involve in many biological functions. To reveal the functions and regulatory mechanisms of lncRNAs, it is vital to understand how lncRNAs regulate their target genes for implementing specific biological functions. In this article, we review the computational methods for inferring lncRNA–mRNA interactions and the third-party databases of storing lncRNA–mRNA regulatory relationships. We have found that the existing methods are based on statistical correlations between the gene expression levels of lncRNAs and mRNAs, and may not reveal gene regulatory relationships which are causal relationships. Moreover, these methods do not consider the modularity of lncRNA–mRNA regulatory networks, and thus, the networks identified are not module-specific. To address the above two issues, we propose a novel method, MSLCRN, to infer and analyze module-specific lncRNA–mRNA causal regulatory networks. We have applied it into glioblastoma multiforme, lung squamous cell carcinoma, ovarian cancer and prostate cancer, respectively. The experimental results show that MSLCRN, as an expression-based method, could be a useful complementary method to study lncRNA regulations.

scholarly journals Prenylated Flavonoids fromMorus albaL. Cause Inhibition of G1/S Transition in THP-1 Human Leukemia Cells and Prevent the Lipopolysaccharide-Induced Inflammatory Response

2013 ◽  
Vol 2013 ◽  
pp. 1-13 ◽  
Author(s):  
Peter Kollar ◽  
Tomáš Bárta ◽  
Jan Hošek ◽  
Karel Souček ◽  
Veronika Müller Závalová ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Inflammatory Response ◽  
Cell Cycle Progression ◽  
Human Cancer ◽  
Biological Effects ◽  
Cell Types ◽  
Human Leukemia ◽  
Cycle Progression ◽  
Prenylated Flavonoids ◽  
Anti Inflammatory

Morus albaL. (MA) is a natural source of many compounds with different biological effects. It has been described to possess anti-inflammatory, antioxidant, and hepatoprotective activities. The aim of this study was to evaluate cytotoxicity of three flavonoids isolated from MA (kuwanon E, cudraflavone B, and4′-O-methylkuwanon E) and to determine their effects on proliferation of THP-1 cells, and on cell cycle progression of cancer cells. Anti-inflammatory effects were also determined for all three given flavonoids. Methods used in the study included quantification of cells by hemocytometer and WST-1 assays, flow cytometry, western blotting, ELISA, and zymography. From the three compounds tested, cudraflavone B showed the strongest effects on cell cycle progression and viability of tumor and/or immortalized cells and also on inflammatory response of macrophage-like cells. Kuwanon E and4′-O-methylkuwanon E exerted more sophisticated rather than direct toxic effect on used cell types. Our data indicate that mechanisms different from stress-related or apoptotic signaling pathways are involved in the action of these compounds. Although further studies are required to precisely define the mechanisms of MA flavonoid action in human cancer and macrophage-like cells, here we demonstrate their effects combining antiproliferative and anti-inflammatory activities, respectively.

scholarly journals Mmu-miR-27a-5p-Dependent Upregulation of MCPIP1 Inhibits the Inflammatory Response in LPS-Induced RAW264.7 Macrophage Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Ying Cheng ◽  
Li Du ◽  
Hanwei Jiao ◽  
Huapei Zhu ◽  
Kailian Xu ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Western Blot ◽  
Proinflammatory Cytokine ◽  
Target Genes ◽  
Noncoding Rnas ◽  
Luciferase Reporter ◽  
Qrt Pcr ◽  
Macrophage Cells ◽  
Reporter Assays ◽  
Raw264.7 Macrophage

Lipopolysaccharide (LPS) stimulates macrophages to release proinflammatory cytokines. MicroRNAs (miRNAs) are short noncoding RNAs that are involved in inflammatory reaction. Our previously study identified the downregulated expression of mmu-miR-27a-5p in RAW267.4 cells treated with LPS. To dissect the mechanism that mmu-miR-27a-5p regulates target genes and affects proinflammatory cytokine secretion more clearly, based on previous bioinformatics prediction data, one of the potential target genes, MCPIP1 was observed to be upregulated with qRT-PCR and western blot. Luciferase reporter assays were performed to further confirmin silicoprediction and determine that MCPIP1 is the target of mmu-miR-27-5p. The results suggested that mmu-miR-27a-5p directly targeted the 3′-UTR of MCPIP1 and the interaction between mmu-miR-27-5p and the 3′-UTR of MCPIP1 is sequence-specific. MCPIP1 overexpression decreased the secretion of IL-6, IL-1β, and IL-10 in macrophage cells stimulated with LPS. Our findings may provide the important information for the precise roles of mmu-miR-27a-5p in the macrophage inflammatory response to LPS stimulation in the future.

scholarly journals Epi-miRNAs: Regulators of the Histone Modification Machinery in Human Cancer

2022 ◽  
Vol 2022 ◽  
pp. 1-22
Author(s):  
Deniz Mortazavi ◽  
Behnoush Sohrabi ◽  
Meysam Mosallaei ◽  
Ziba Nariman-Saleh-Fam ◽  
Milad Bastami ◽  
...  
Keyword(s):  
Histone Modification ◽  
Cell Fate ◽  
Target Genes ◽  
Human Cancer ◽  
Noncoding Rnas ◽  
Fine Tuning ◽  
Small Noncoding Rnas ◽  
Histone Modifiers ◽  
Histone Modifying Enzymes

Cancer is a leading cause of death and disability worldwide. Epigenetic deregulation is one of the most critical mechanisms in carcinogenesis and can be classified into effects on DNA methylation and histone modification. MicroRNAs are small noncoding RNAs involved in fine-tuning their target genes after transcription. Various microRNAs control the expression of histone modifiers and are involved in a variety of cancers. Therefore, overexpression or downregulation of microRNAs can alter cell fate and cause malignancies. In this review, we discuss the role of microRNAs in regulating the histone modification machinery in various cancers, with a focus on the histone-modifying enzymes such as acetylases, deacetylases, methyltransferases, demethylases, kinases, phosphatases, desumoylases, ubiquitinases, and deubiquitinases. Understanding of microRNA-related aberrations underlying histone modifiers in pathogenesis of different cancers can help identify novel therapeutic targets or early detection approaches that allow better management of patients or monitoring of treatment response.

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