A new miRNA regulator, miR-672, reduces cardiac hypertrophy by inhibiting JUN expression

Lü, Yifei; Wu, Fuyong

doi:10.1016/j.gene.2018.01.047

Cited by 13 publications

(7 citation statements)

References 47 publications

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“…MiR-10a inhibits cardiac hypertrophy by downregulating the expression of T-box5, a transcription factor involved in cardiac development [61]. Both miR-672-5p and miR-139-5p ameliorate cardiac hypertrophy in cardiomyocytes by inhibiting the expression of another transcription factor c-Jun, a subunit of activator protein-1 (AP-1) [68,69]. Similarly, miR-150 mimics were shown to abrogate glucose-induced cardiomyocyte hypertrophy by repressing the expression of p300, a cofactor for various hypertrophy-responsive transcription factors [70].…”

Section: Micrornas That Promote Cardiac Hypertrophymentioning

confidence: 99%

MicroRNAs in Cardiac Hypertrophy

Wehbe

Nasser

Pintus

et al. 2019

IJMS

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Like other organs, the heart undergoes normal adaptive remodeling, such as cardiac hypertrophy, with age. This remodeling, however, is intensified under stress and pathological conditions. Cardiac remodeling could be beneficial for a short period of time, to maintain a normal cardiac output in times of need; however, chronic cardiac hypertrophy may lead to heart failure and death. MicroRNAs (miRNAs) are known to have a role in the regulation of cardiac hypertrophy. This paper reviews recent advances in the field of miRNAs and cardiac hypertrophy, highlighting the latest findings for targeted genes and involved signaling pathways. By targeting pro-hypertrophic genes and signaling pathways, some of these miRNAs alleviate cardiac hypertrophy, while others enhance it. Therefore, miRNAs represent very promising potential pharmacotherapeutic targets for the management and treatment of cardiac hypertrophy.

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Section: Micrornas That Promote Cardiac Hypertrophymentioning

confidence: 99%

MicroRNAs in Cardiac Hypertrophy

Wehbe

Nasser

Pintus

et al. 2019

IJMS

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“…Two miRNAs involved in cardiovascular development (miR-3065) and in the regulation of cardiac hyperthrophy (miR-672) were also upregulated by licofelone. miR-672 showed suppressive effects on cardiac hypertrophy through regulating the expression of Jun in cardiomyocytes (46). As mentioned in the Introduction, targeting both COX and 5-LOX pathways may avoid cardiovascular side effects (17), and 5-LOX has been identified as a major gene contributing to atherosclerosis susceptibility in mice (47).…”

Section: Discussionmentioning

confidence: 99%

Modulation of smoke-induced DNA and microRNA alterations in mouse lung by licofelone, a triple COX-1, COX-2 and 5-LOX inhibitor

Izzotti

Balansky²,

Micale

et al. 2019

Carcinogenesis

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Chronic inflammation plays a crucial role in the carcinogenesis process and, in particular, in smoking-related carcinogenesis. Therefore, anti-inflammatory agents provide an interesting perspective in the prevention of smoking-associated cancers. Among nonsteroidal anti-inflammatory drugs (NSAIDs), licofelone is a triple inhibitor of both cyclooxygenases (COX-1 and COX-2) and of 5-lipooxygenase (5-LOX) that has shown some encouraging results in cancer prevention models. We previously showed that the dietary administration of licofelone, starting after weanling, to Swiss H mice exposed for 4 months to mainstream cigarette smoke since birth attenuated preneoplastic lesions of inflammatory nature in both lung and urinary tract, and had some effects on the yield of lung tumors at 7.5 months of age. The present study aimed at evaluating the early modulation by licofelone of pulmonary DNA and RNA alterations either in smoke-free or smoke-exposed H mice after 10 weeks of exposure. Licofelone protected the mice from the smoke-induced loss of body weight and significantly attenuated smoke-induced nucleotide alterations by decreasing the levels of bulky DNA adducts and 8-hydroxy-2′-deoxyguanosine in mouse lung. Moreover, the drug counteracted dysregulation by smoke of several pulmonary microRNAs involved in stress response, inflammation, apoptosis, and oncogene suppression. However, even in smoke-free mice administration of the drug had significant effects on a broad panel of microRNAs and, as assessed in a subset of mice used in a parallel cancer chemoprevention study, licofelone even enhanced the smoke-induced systemic genotoxic damage after 4 months of exposure. Therefore, caution should be paid when administering licofelone to smokers for long periods.

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“…A total of 10 established miRNA-target prediction programs (Diana-microT, miRanda, miRDB, miRWalk, RNAhybrid, PICTAR4, PICTAR5, PITA, RNA22 and TargetScan) were available in miRWalk. The potential targets of one miRNA are considered to be the genes that have been predicted by at least 5 programs (21). …”

Section: Methodsmentioning

confidence: 99%

MicroRNA‑144 mediates chronic inflammation and tumorigenesis in colorectal cancer progression via regulating C‑X‑C motif chemokine ligand 11

Han

Feng

Yu³

et al. 2018

Exp Ther Med

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Colorectal cancer (CRC) is one of the most common malignancies worldwide. The aim of the present study was to investigate the expression of microRNA-144 (miR-144) and C-X-C motif chemokine ligand 11 (CXCL11) in CRC and their association. Data from Gene Expression Omnibus (GEO) DataSets were analyzed to obtain the expression profile of CXCL11 in CRC. Subsequently, serum samples were collected from 65 subjects, including 39 patients with CRC and 26 controls; CRC and adjacent normal tissues were collected from all 39 CRC patients and the expression of CXCL11 was measured in these specimens. After searching for the potential regulator of CXCL11 through bioinformatics analysis, the levels of miR-144 in the clinical specimens were also detected. Finally, the regulatory association between miR-144 and CXCL11 was certified via the dual-luciferase reporter assay. Microarray data and bioinformatics analysis demonstrated that CXCL11 was significantly upregulated in CRC tissues and miR-144 was a potential regulator of CXCL11. In line with this finding, the expression of CXCL11 was significantly increased in the serum and tumor samples of patients with CRC, while that of miR-144 was downregulated. Dual-luciferase reporter assay revealed that miR-144 directly targets the 3′-untranslated region of CXCL11 mRNA to regulate its expression. These results demonstrated that enhanced CXCL11 expression in patients with CRC was associated with reduced miR-144 expression. The results of the present study may indicate a novel regulatory role of miR-144 in CRC through CXCL11 downregulation.

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A new miRNA regulator, miR-672, reduces cardiac hypertrophy by inhibiting JUN expression

Cited by 13 publications

References 47 publications

MicroRNAs in Cardiac Hypertrophy

MicroRNAs in Cardiac Hypertrophy

Modulation of smoke-induced DNA and microRNA alterations in mouse lung by licofelone, a triple COX-1, COX-2 and 5-LOX inhibitor

MicroRNA‑144 mediates chronic inflammation and tumorigenesis in colorectal cancer progression via regulating C‑X‑C motif chemokine ligand 11

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