MiR-19a regulates PTEN expression to mediate glycogen synthesis in hepatocytes

Dou, Lin; Meng, Xiangyu; Sui, Xiaofang; Wang, Shuyue; Shen, Tao; Huang, Xiuqing; Guo, Jun; Fang, Weiwei; Man, Yong; Xi, Jianzhong; Li, Jian

doi:10.1038/srep11602

Cited by 41 publications

(36 citation statements)

References 25 publications

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“…For example, miR-200s contributed to IL-6-induced insulin resistance in hepatocytes22. MiR-19a regulated PTEN expression to mediate glycogen synthesis in hepatocytes23. In addition, we demonstrated that the expression of miR-291b-3p was significantly upregulated in db/db and HFD-fed mice.…”

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confidence: 68%

Hepatic MiR-291b-3p Mediated Glucose Metabolism by Directly Targeting p65 to Upregulate PTEN Expression

Guo

Dou

Meng

et al. 2017

Sci Rep

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Several studies have suggested an important role of miR-291b-3p in the development of embryonic stem cells. In previous study, we found that the expression of miR-291b-3p was significantly upregulated in the liver of db/db mice. However, the role of miR-291b-3p in glucose metabolism and its underlying mechanisms remain unknown. In the present study, we demonstrated that miR-291b-3p was abundantly expressed in the liver. Of note, hepatic miR-291b-3p expression was upregulated in HFD-fed mice and induced by fasting in C57BL/6 J normal mice. Importantly, hepatic inhibition miR-291b-3p expression ameliorated hyperglycemia and insulin resistance in HFD-fed mice, whereas hepatic overexpression of miR-291b-3p led to hyperglycemia and insulin resistance in C57BL/6 J normal mice. Further study revealed that miR-291b-3p suppressed insulin-stimulated AKT/GSK signaling and increased the expression of gluconeogenic genes in hepatocytes. Moreover, we identified that p65, a subunit of nuclear factor-κB (NF-κB), is a target of miR-291b-3p by bioinformatics analysis and luciferase reporter assay. Silencing of p65 significantly augmented the expression of PTEN and impaired AKT activation. In conclusion, we found novel evidence suggesting that hepatic miR-291b-3p mediated glycogen synthesis and gluconeogenesis through targeting p65 to regulate PTEN expression. Our findings indicate the therapeutic potential of miR-291b-3p inhibitor in hyperglycemia and insulin resistance.

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confidence: 68%

Hepatic MiR-291b-3p Mediated Glucose Metabolism by Directly Targeting p65 to Upregulate PTEN Expression

Guo

Dou

Meng

et al. 2017

Sci Rep

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“…Aberrant PTEN expression or activation has been reported in many cancer types [28,29]. Moreover, miRNAs were also identified as novel regulators for PTEN, and these miRNAs include miR-19a [30], miR-21 [31], miR-26a [32], and miR-214 [33]. It is notable that overexpression of these PTEN-targeting miRNAs targeting was considered as a contributing factor for tumor development in these reports [32].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-152 Targets Phosphatase and Tensin Homolog to Inhibit Apoptosis and Promote Cell Migration of Nasopharyngeal Carcinoma Cells

Huang

Zhu

2016

Med Sci Monit

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BackgroundNasopharyngeal carcinoma (NPC) is a type of head and neck cancer with very high prevalence in southern China. Phosphatase and tensin homolog (PTEN), a tumor suppressor, was reported to be downregulated in NPC patients and correlated with pathological grade and clinical stage of NPC.Material/MethodsLuciferase reporter assay, qPCR, and Western blot analysis were used to determine if PTEN is a target of miR-152. The function of miR-152 in cell apoptosis and cell proliferation was examined as well. Tissue samples from NPC patients were also analyzed for PTEN and miR-152 expressions.ResultsReporter assay indicated miR-152 targets the 3′UTR of PTEN mRNA to inhibit PTEN expression. Transfection of the NPC-derived cell line with miR-152 mimic confirmed these findings. Overexpression of miRNA-152 inhibits apoptosis induced by Cisplatin in NPC cancer cells in vitro. Moreover, overexpression miR-152 also promotes NPC cancer cell invasion and proliferation. Samples from EBV-negative NPC patients demonstrated the down-regulated level of PTEN may be related with overexpression of miR-152.ConclusionsThe miR-152 targets PETN to inhibit cell apoptosis and promote cancer cell proliferation and migration in NPC development.

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“…Dysregulation of PTEN expression and activation has been reported in many cancers (Li et al, 1997;Chen et al, 2005). Several miRNAs, such as miR-19a (Dou et al, 2015), miR-21 (Qi et al, 2009), miR-26a (Huse et al, 2009), and miR-214 (Schwarzenbach et al, 2012) have been identified as regulators of PTEN expression. In these reports, overexpression of miRNAs targeting PTEN has been considered a contributing factor for tumor development (Huse et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

A microRNA-152 that targets the phosphatase and tensin homolog to inhibit low oxygen induced-apoptosis in human brain microvascular endothelial cells

Cao

et al. 2016

Genet. Mol. Res.

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ABSTRACT. Brain damage caused by perinatal asphyxia is dangerous for neonatal infants, but the mechanism by which it occurs remains elusive. In this study, microRNA-152 (miR-152) expression was induced by low oxygen levels in rat models of hypoxia brain damage, as well as in human brain microvascular endothelial cells (HBMECs) cultured in vitro. Analysis of the sequence of miR-152 revealed that the phosphatase and tensin homolog gene (PTEN) is probably the target of miR-152 both in humans and rats. When HBMECs were transfected with miR-152 mimics, PTEN expression was inhibited at both the mRNA and protein levels. Moreover, transfection with the miR-152 mimic also inhibited apoptosis induced by hypoxia. Furthermore, expression of the pro-apoptotic gene Bax was downregulated while the anti-apoptotic gene Bcl2 was upregulated after miR-152 mimic transfection. Taken together, these results indicate that miR-152 induced by hypoxia suppresses cell apoptosis and acts as a protective factor during hypoxia by repressing PTEN.

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MiR-19a regulates PTEN expression to mediate glycogen synthesis in hepatocytes

Cited by 41 publications

References 25 publications

Hepatic MiR-291b-3p Mediated Glucose Metabolism by Directly Targeting p65 to Upregulate PTEN Expression

Hepatic MiR-291b-3p Mediated Glucose Metabolism by Directly Targeting p65 to Upregulate PTEN Expression

MicroRNA-152 Targets Phosphatase and Tensin Homolog to Inhibit Apoptosis and Promote Cell Migration of Nasopharyngeal Carcinoma Cells

A microRNA-152 that targets the phosphatase and tensin homolog to inhibit low oxygen induced-apoptosis in human brain microvascular endothelial cells

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