Down‐regulation of miR‐146a‐5p and its potential targets in hepatocellular carcinoma validated by a <scp>TCGA</scp>‐ and <scp>GEO</scp>‐based study

Zhang, Daniel Xin; Ye, Zhihua; Liang, Hai‐Wei; Ren, Fanghui; Li, Ping; Dang, Yi‐Wu; Chen, Gang

doi:10.1002/2211-5463.12198

Cited by 34 publications

(29 citation statements)

References 43 publications

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“…miR-146a-5p functions as a tumor suppressor in various types of cancer, including hepatocellular carcinoma, esophageal squamous cell carcinoma, NSCLC and prostate cancer (20)(21)(22)(23). However, the role of miR-146a-5p in the development of TNBC remains unclear.…”

Section: Discussionmentioning

confidence: 99%

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Effect of miR-146a-5p on proliferation and metastasis of triple-negative breast cancer via regulation of SOX5

Yao

2018

Exp Ther Med

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Abstract. MicroRNA (miR)-146a-5p functions as a tumor suppressor in various types of cancer. However, the role of miR-146a-5p in the development of triple-negative breast cancer (TNBC) is unclear. The present study aimed to investigate the role of miR-146a-5p in TNBC. The expression level of miR-146a-5p in TNBC tissues and cell lines was initially detected using reverse transcription-quantitative polymerase chain reaction. To predict the target gene of miR-146a-5p, TargetScan software was used and a dual luciferase assay was performed to verify the prediction. Furthermore, in order to explore the role of miR-146a-5p in TNBC, miR-146a-5p was overexpressed in TNBC cells using miR-146a-5p mimics. An MTT assay was performed to detect cell proliferation, and a Transwell assay was conducted to determine cell migration and invasion. Furthermore, western blotting was performed to measure associated protein expression. It was revealed that miR-146a-5p was downregulated in TNBC tissues and cell lines. SOX5 was indicated to be a target gene of miR-146a-5p and was upregulated in TNBC cells. Additionally, miR-146a-5p could inhibit TNBC cell proliferation, migration and invasion, repress the expression of mesenchymal markers (N-cadherin, vimentin and fibronectin) and increase epithelial marker (E-cadherin) expression. Furthermore, SOX5 overexpression eliminated the effects of miR-146a-5p mimics on TNBC cells. In conclusion, the data of the present study indicated that miR-146a-5p inhibits the proliferation and metastasis of TNBC cells by regulating SOX5.

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Section: Discussionmentioning

confidence: 99%

“…Zhang et al (20) reported that miR-146a-5p was downregulated in hepatocellular carcinoma and acted as a tumor suppressor. Wang et al (21) revealed that miR-146a-5p promoted esophageal squamous cell carcinoma progression by regulating epithelial-mesenchymal transition (EMT) via targeting Notch2.…”

Section: Introductionmentioning

confidence: 99%

Effect of miR-146a-5p on proliferation and metastasis of triple-negative breast cancer via regulation of SOX5

Yao

2018

Exp Ther Med

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“…Jin et al reported that miR-146a was significantly decreased in non-alcoholic steatohepatits (NASH) and that overexpression of miR-146a was capable of improving NASH by targeting HdMcP (27). In addition, miR-146a has been found to play an important role in liver cancer (28)(29)(30). However, there are few literature reports regarding whether miR-146a plays a role in the development of insulin resistance and NAFLd.…”

Section: Mir-146a Improves Hepatic Lipid and Glucose Metabolism By Tamentioning

confidence: 99%

miR‑146a improves hepatic lipid and glucose metabolism by targeting MED1

Bao

Wei

et al. 2019

Int J Mol Med

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Non-alcoholic fatty liver disease (NAFLd) is one of the most common chronic liver diseases worldwide. Increasing evidence has shown that microRNAs (miRNAs) play a vital role in the progression of NAFLd. The aim of the present study was to examine the expression level and roles of miR-146a in fatty liver of high-fat diet (HFd) and ob/ob mice and fatty acid-treated hepatic cells using RT-qPcR and western blot analysis. The results showed that the expression of miR-146a was significantly decreased in the livers of high-fat diet (HFd) and ob/ob mice and free fatty acid-stimulated cells by RT-qPcR. Overexpression of hepatic miR-146a improved glucose and insulin tolerance as well as lipid accumulation in the liver by promoting the oxidative metabolism of fatty acids. In addition, the overexpression of miR-146a increased the amount of mitochondria and promoted mitochondrial respiration in hepatocytes. Similarly, inhibition of miR-146a expression levels significantly reduced mitochondrial numbers in AML12 cells as well as the expression of mitochondrial respiration related genes. Additionally, MEd1 was a direct target of miR-146a and restoring MEd1 abolished the metabolic effects of miR-146a on lipid metabolism and mitochondrial function. Therefore, results of the present study identified a novel function of miR-146a in glucose and lipid metabolism in targeting MEd1, suggesting that miR-146a serves as a potential therapeutic target for metabolic syndrome disease.

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“…Intracranial aneurysms [111], coronary heart disease [112], myocardial infarction [113], myocardial hypertrophy [114], dilated cardiomyopathy [115], pulmonary arterial hypertension [116], acute ischemic stroke [89], ascending aortic aneurysm [49] hsa-miR-145-5p 5q33 Hypertension [117,118], dilated cardiomyopathy [119], myocardial infarction [120,121], stroke [121], acute cerebral ischemic/reperfusion [122], T2DM [24,123], T1DM [52], diabetic retinopathy [124], gestational diabetes mellitus [125] hsa-miR-146a-5p 5q33.3 [126,127] Angiogenesis [128], hypoxia, ischemia/reperfusion-induced cardiac injury [129], myocardial infarction [17], coronary atherosclerosis, coronary heart disease in patients with subclinical hypothyroidism [130], acute ischemic stroke, acute cerebral ischemia [131], T2DM [24,52], T1DM [75], diabetic nephropathy [57] hsa-miR-181a-5p 1q32.1 9q33.3 [132] Regulation of hypertension-related genes [50], atherosclerosis [132], metabolic syndrome, coronary artery disease [133], non-alcoholic fatty liver disease [134], ischaemic stroke, transient ischaemic attack, acute myocardial infarction [135,136], obesity and insulin resistance [62,…”

Section: Introductionmentioning

confidence: 99%

Diabetes Mellitus and Cardiovascular Risk Assessment in Mothers with a History of Gestational Diabetes Mellitus Based on Postpartal Expression Profile of MicroRNAs Associated with Diabetes Mellitus and Cardiovascular and Cerebrovascular Diseases

Hromadníková

Dvořáková

Krofta

2020

IJMS

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Mothers with a history of gestational diabetes mellitus (GDM) have an increased risk of developing diabetes in the future and a lifelong cardiovascular risk. Postpartal expression profile of cardiovascular/cerebrovascular disease associated microRNAs was assessed 3–11 years after the delivery in whole peripheral blood of young and middle-aged mothers with a prior exposure to GDM with the aim to identify a high-risk group of mothers at risk of later development of diabetes mellitus and cardiovascular/cerebrovascular diseases who would benefit from implementation of early primary prevention strategies and long-term follow-up. The hypothesis of the assessment of cardiovascular risk in women was based on the knowledge that a series of microRNAs play a role in the pathogenesis of diabetes mellitus and cardiovascular/cerebrovascular diseases. Abnormal expression profile of multiple microRNAs was found in women with a prior exposure to GDM (miR-1-3p, miR-16-5p, miR-17-5p, miR-20a-5p, miR-20b-5p, miR-21-5p, miR-23a-3p, miR-24-3p, miR-26a-5p, miR-29a-3p, miR-100-5p, miR-103a-3p, miR-125b-5p, miR-126-3p, miR-130b-3p, miR-133a-3p, miR-143-3p, miR-145-5p, miR-146a-5p, miR-181a-5p, miR-195-5p, miR-199a-5p, miR-221-3p, miR-342-3p, miR-499a-5p, and-miR-574-3p). Postpartal combined screening of miR-1-3p, miR-16-5p, miR-17-5p, miR-20b-5p, miR-21-5p, miR-23a-3p, miR-26a-5p, miR-29a-3p, miR-103a-3p, miR-133a-3p, miR-146a-5p, miR-181a-5p, miR-195-5p, miR-199a-5p, miR-221-3p, and miR-499a-5p showed the highest accuracy for the identification of mothers with a prior exposure to GDM at a higher risk of later development of cardiovascular/cerebrovascular diseases (AUC 0.900, p < 0.001, sensitivity 77.48%, specificity 93.26%, cut off >0.611270413). It was able to identify 77.48% mothers with an increased cardiovascular risk at 10.0% FPR. Any of changes in epigenome (upregulation of miR-16-5p, miR-17-5p, miR-29a-3p, and miR-195-5p) that were induced by GDM-complicated pregnancy are long-acting and may predispose mothers affected with GDM to later development of diabetes mellitus and cardiovascular/cerebrovascular diseases. In addition, novel epigenetic changes (upregulation of serious of microRNAs) appeared in a proportion of women that were exposed to GDM throughout the postpartal life. Likewise, a previous occurrence of either GH, PE, and/or FGR, as well as a previous occurrence of GDM, is associated with the upregulation of miR-1-3p, miR-17-5p, miR-20a-5p, miR-20b-5p, miR-29a-3p, miR-100-5p, miR-125b-5p, miR-126-3p, miR-130b-3p, miR-133a-3p, miR-143-3p, miR-145-5p, miR-146a-5p, miR-181a-5p, miR-199a-5p, miR-221-3p, and miR-499a-5p. On the other hand, upregulation of miR-16-5p, miR-21-5p, miR-23a-3p, miR-24-3p, miR-26a-5p, miR-103a-3p, miR-195-5p, miR-342-3p, and miR-574-3p represents a unique feature of aberrant expression profile of women with a prior exposure to GDM. Screening of particular microRNAs may stratify a high-risk group of mothers with a history of GDM who might benefit from implementation of early primary prevention strategies.

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Down‐regulation of miR‐146a‐5p and its potential targets in hepatocellular carcinoma validated by a TCGA‐ and GEO‐based study

Cited by 34 publications

References 43 publications

Effect of miR-146a-5p on proliferation and metastasis of triple-negative breast cancer via regulation of SOX5

Effect of miR-146a-5p on proliferation and metastasis of triple-negative breast cancer via regulation of SOX5

miR‑146a improves hepatic lipid and glucose metabolism by targeting MED1

Diabetes Mellitus and Cardiovascular Risk Assessment in Mothers with a History of Gestational Diabetes Mellitus Based on Postpartal Expression Profile of MicroRNAs Associated with Diabetes Mellitus and Cardiovascular and Cerebrovascular Diseases

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