miRNAs Regulate hERG

Lian, Jing; Guo, Jian; Huang, Xiaoyan; Yang, Xi; Huang, Guochang; Mao, Haiyan; Sun, Huan; Ba, Yanna; Zhou, Jian

doi:10.1111/jce.13084

Cited by 10 publications

(2 citation statements)

References 47 publications

(80 reference statements)

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“…Previous study has shown that a kind of cells expressing high level of the fatty acid receptor CD36 has been found in human oral cancer samples, and they have a high metastatic potential in mice [34]. miRNAs play an important regulatory role in post-transcriptional regulation of gene expression, and participate in a variety of biological processes including intercellular signal transmission, cell proliferation, growth, differentiation, apoptosis, and cell metabolism [35]. Recent studies have found that miRNA plays an important role in energy metabolism such as glucose metabolism, fat metabolism and amino acid metabolism [36, 37].…”

Section: Discussionmentioning

confidence: 99%

miR-21 promotes non-small cell lung cancer cells growth by regulating fatty acid metabolism

Wang

et al. 2019

Cancer Cell Int

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Background Lung cancer is one of the most common malignant tumors worldwide. CD36 is a receptor for fatty acids and plays an important role in regulating fatty acid metabolism, which is closely related to tumorigenesis and development. The regulation of miR-21 and its role in tumorigenesis have been extensively studied in recent years. However, the relationship between miR-21 and CD36 regulated fatty acid metabolism in human non-small cell lung cancer remains unknown. Methods In this study, lentivirus transfection, qRT-PCR, cell migration, immunofluorescence, and western blot were used to examine the relationship between miR-21 and CD36 regulated fatty acid metabolism and the regulation role of miR-21 in human non-small cell lung cancer. Results This study demonstrated that up-regulation of miR-21 promoted cell migration and cell growth in human non-small cell lung cancer cells. Moreover, the intracellular contents of lipids including cellular content of phospholipids, neutral lipids content, cellular content of triglycerides were significantly increased following miR-21 mimic treatment compared with control, and the levels of key lipid metabolic enzymes FASN, ACC1 and FABP5 were obviously enhanced in human non-small cell lung cancer cells. Furthermore, down-regulation of CD36 suppressed miR-21 regulated cell growth, migration and intracellular contents of lipids in human non-small cell lung cancer cells, which suggested that miR-21 promoted cell growth and migration of human non-small cell lung cancer cells through CD36 mediated fatty acid metabolism. Inhibition of miR-21 was revealed to inhibit cell growth, migration, intracellular contents of lipids, and CD36 protein expression level in human non-small cell lung cancer cells. In addition, PPARGC1B was a direct target of miR-21, and down-regulation of PPARGC1B reversed the inhibition of CD36 expression induced by miR-21 inhibitor. Conclusions These results explored the mechanism of miR-21 promoted non-small cell lung cancer and might provide a novel therapeutic method in treating non-small cell lung cancer in clinic.

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Section: Discussionmentioning

confidence: 99%

miR-21 promotes non-small cell lung cancer cells growth by regulating fatty acid metabolism

Wang

et al. 2019

Cancer Cell Int

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“…The ether-a-go-go-related gene (hERG) is the major molecular component of the rapidly activating delayed rectifier K + current (Ikr) and it is also modulated by miRNAs in LQTS. By coupling in silico and in vitro studies, Lian et al correlated miR-134, miR-103a-1, miR-143, and miR-3619 overexpression with the downregulation of hERG mRNA and protein [67]. Moreover, the current activation and tail amplitude of hERG channel was reduced upon the increase of miR-103a-1 levels.…”

Section: Mirnas and Inherited Cardiomyopathiesmentioning

confidence: 99%

MicroRNAs in Cardiac Diseases

Colpaert

Calore

2019

Cells

150

117

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Since their discovery 20 years ago, microRNAs have been related to posttranscriptional regulation of gene expression in major cardiac physiological and pathological processes. We know now that cardiac muscle phenotypes are tightly regulated by multiple noncoding RNA species to maintain cardiac homeostasis. Upon stress or various pathological conditions, this class of non-coding RNAs has been found to modulate different cardiac pathological conditions, such as contractility, arrhythmia, myocardial infarction, hypertrophy, and inherited cardiomyopathies. This review summarizes and updates microRNAs playing a role in the different processes underlying the pathogenic phenotypes of cardiac muscle and highlights their potential role as disease biomarkers and therapeutic targets.

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