MicroRNA-449 suppresses proliferation of hepatoma cell lines through blockade lipid metabolic pathway related to SIRT1

Zhang, Hongyi; Feng, Zhiqiang; Huang, Rui; Xia, Zhenglin; Xiang, Guoan; Zhang, Jinqian

doi:10.3892/ijo.2014.2596

Cited by 48 publications

(39 citation statements)

References 73 publications

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“…SIRT1 could affect growth arrest, cell death, DNA damage repair, and metabolism and is associated with life span and cancer risk . SIRT1 may play as an oncogene or a suppressor in tumor based on the previous studies.…”

Section: Discussionmentioning

confidence: 99%

miR‐204‐5p targeting SIRT1 regulates hepatocellular carcinoma progression

Jiang

Wen

Zheng

et al. 2016

Cell Biochemistry & Function

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Hepatocellular carcinoma (HCC) is the most common type of cancer, which presents rapid tumor growth, drug resistance, and metastasis. Recently, microRNAs are shown to be involved in the cell biological processes in HCC, but the underlying molecular mechanisms remain unclear. This study aimed to investigate the cellular function and molecular mechanism of miR-204-5p in HCC. SIRT1 mRNA and miR-204-5p were examined by real-time reverse transcription polymerase chain reaction. SIRT1 protein levels were measured by Western blotting. Cell proliferation assay was performed to confirm colony formation. Invasion assay was performed by transwell system. SPSS 15.0 for Windows was used for statistical analysis. SIRT1 was a potential oncogene in cancer, which was identified as a direct target of miR-204-5p. Overexpression of miR-204-5p in human HCC cell lines (BEL-7405 and QGY-7701) caused the suppression of cell survival ability, the increase of apoptosis, and drug sensitivity. SIRT1 was overexpressed in human HCC tissues and was negatively related to miR-204-5p levels. These results indicate that miR-204-5p and SIRT1 may play an important role in the development of HCC.

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Section: Discussionmentioning

confidence: 99%

miR‐204‐5p targeting SIRT1 regulates hepatocellular carcinoma progression

Jiang

Wen

Zheng

et al. 2016

Cell Biochemistry & Function

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“…miR-34 was confirmed to be a tumor suppressor, and its level was relatively low in the cardiovascular system. Similarly, previous studies also suggested that miR-449a was a tumor suppressor in numerous cancer types by targeting different target genes [8, 26, 27]. Moreover, a number of studies recently indicated the downregulation of the expression of miR-449 in various human malignancies, including lung cancer, prostate cancer, and adrenal hyperplasia [28, 29].…”

Section: Discussionmentioning

confidence: 99%

“…MicroRNAs (miRNAs) are small noncoding RNAs that specifically bind to target mRNAs and thus downregulate gene expression by degradation or translational repression [8, 9]. Recently, these molecules have been implicated in several processes of direct relevance to the heart, including cardiac development, cardiac hypertrophy, heart failure, and angiogenesis [10-13].…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-449a Inhibition Protects H9C2 Cells Against Hypoxia/Reoxygenation-Induced Injury by Targeting the Notch-1 Signaling Pathway

Cheng¹,

Wu²,

Rong³

et al. 2018

Cell Physiol Biochem

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Background/Aims: The present study aimed to detect the expression of miR-449a and investigate the effect of miR-449a on cell injury in cardiomyocytes subjected to hypoxia/ reoxygenation (H/R) and its underlying mechanisms. Methods: The expression of miR-449a was determined using reverse transcription–polymerase chain reaction in both neonatal rat ventricular myocytes and H9C2 cells. For gain-of-function and loss-of-function studies, H9C2 cells were transfected with either miR-449a mimics or miR-449a inhibitor. The target gene of miR-449a was confirmed by a dual-luciferase reporter assay. Apoptosis was analyzed by both flow cytometry using Annexin V and propidium iodide and transferase-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL). Necrosis was confirmed by the detection of lactate dehydrogenase release. The cell viability was measured using the methylthiotetrazole method. The protein levels of Notch-1, Notch-1 intracellular domain, hairy and enhancer of split-1 (Hes-1), and apoptosis-related genes were measured by Western blot analysis. Results: MiR-449a was significantly upregulated in both neonatal rat ventricular myocytes and H9C2 cells subjected to H/R. However, H/R-induced cell apoptosis and necrosis were markedly reduced by miR-449a inhibition. By targeting Notch-1, miR-449a regulated the Notch-1/ Hes-1 signaling pathway. The blockade of the Notch signaling pathway partly abolished the protective effect of miR-449a suppression against H/R injury, whereas the overexpression of Notch-1 intracellular domain partly reversed the effect of miR-449a overexpression on H/R-induced cell injury. Conclusions: The present study suggested that miR-449a inhibition protected H9C2 cells against H/R-induced cell injury by targeting the Notch-1 signaling pathway, providing a novel insight into the molecular basis of myocardial ischemia–reperfusion injury and a potential therapeutic target.

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“…SIRT1 increases the level of LXR [38] and decreases SREBP [40]; remarkably, SIRT1 itself is targeted by miR-34a [41, 42], miR-132 [43], miR-204-5p [44], miR-499 [45], and many others.…”

Section: Micrornas Involvement In Lipid Metabolismmentioning

confidence: 99%

Mechanistic Role of MicroRNAs in Coupling Lipid Metabolism and Atherosclerosis

Novák

Olejníčková

Tkáčová

et al. 2015

Advances in Experimental Medicine and Biology

104

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MicroRNAs (miRNAs, miRs) represent a group of powerful and versatile posttranscriptional regulators of gene expression being involved in the fine control of a plethora of physiological and pathological processes. Besides their well-established crucial roles in the regulation of cell cycle, embryogenesis or tumorigenesis, these tiny molecules have also been shown to participate in the regulation of lipid metabolism. In particular, miRs orchestrate cholesterol and fatty acids synthesis, transport, and degradation and low-density and high-density lipoprotein (LDL and HDL) formation. It is thus not surprising that they have also been reported to affect the development and progression of several lipid metabolism-related disorders including liver steatosis and atherosclerosis. Mounting evidence suggests that miRs might represent important “posttranscriptional hubs” of lipid metabolism, which means that one miR usually targets 3′-untranslated regions of various mRNAs that are involved in different steps of one precise metabolic/signaling pathway, e.g., one miR targets mRNAs of enzymes important for cholesterol synthesis, degradation, and transport. Therefore, changes in the levels of one key miR affect various steps of one pathway, which is thereby promoted or inhibited. This makes miRs potent future diagnostic and even therapeutic tools for personalized medicine. Within this chapter, the most prominent microRNAs involved in lipid metabolism, e.g., miR-27a/b, miR-33/33*, miR-122, miR-144, or miR-223, and their intracellular and extracellular functions will be extensively discussed, in particular focusing on their mechanistic role in the pathophysiology of atherosclerosis. Special emphasis will be given on miR-122, the first microRNA currently in clinical trials for the treatment of hepatitis C and on miR-223, the most abundant miR in lipoprotein particles.

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MicroRNA-449 suppresses proliferation of hepatoma cell lines through blockade lipid metabolic pathway related to SIRT1

Cited by 48 publications

References 73 publications

miR‐204‐5p targeting SIRT1 regulates hepatocellular carcinoma progression

miR‐204‐5p targeting SIRT1 regulates hepatocellular carcinoma progression

MicroRNA-449a Inhibition Protects H9C2 Cells Against Hypoxia/Reoxygenation-Induced Injury by Targeting the Notch-1 Signaling Pathway

Mechanistic Role of MicroRNAs in Coupling Lipid Metabolism and Atherosclerosis

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