MiR-291b-3p Induces Apoptosis in Liver Cell Line NCTC1469 by Reducing the Level of RNA-binding Protein HuR

Guo, Jun; Li, Meng; Meng, Xiangyu; Sui, Jingzhe; Dou, Lin; Tang, Weiqing; Huang, Xiuqing; Man, Yong; Wang, Shu; Li, Jian

doi:10.1159/000358654

Cited by 34 publications

(41 citation statements)

References 44 publications

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“…Recently, miR-122, miR-33, miR-30c, miR-24, and miR-130 have been identified as important regulators of lipid metabolism (18 -22). In a previous microarray screening, we found that miR-291b-3p was in-creased in the steatotic liver of db/db mice (23). MiR-291b-3p is in the murine miR-290 cluster, and previous studies have suggested a role for this miRNA in the development of embryonic stem cells (24 -26).…”

mentioning

confidence: 81%

“…Transfection of miRs or siRNA was performed with HiPerFect transfection reagent (Qiagen) as previously described (23).…”

Section: Methodsmentioning

confidence: 99%

“…No studies have linked miR-291b-3p to hepatic lipid accumulation. Considering its substantial increase in steatotic livers (23), in the present study, we examined whether miR-291b-3p regulates hepatic lipid metabolism. We found that miR-291b-3p promotes hepatic lipid accumulation by stimulating hepatic lipogenesis.…”

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confidence: 99%

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Liver MicroRNA-291b-3p Promotes Hepatic Lipogenesis through Negative Regulation of Adenosine 5′-Monophosphate (AMP)-activated Protein Kinase α1

Meng

Guo

Fang

et al. 2016

Journal of Biological Chemistry

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In a microarray study, we found that hepatic miR-291b-3p was significantly increased in leptin-receptor-deficient type 2 mice (db/db), a mouse model of diabetes. The function of miR291b-3p is unknown. The potential role of miR-291b-3p in regulating hepatic lipid metabolism was explored in this study. High-fat diet (HFD)-and chow-fed mice were injected with an adenovirus expressing a miR-291b-3p inhibitor and a miR291b-3p mimic through the tail vein. Hepatic lipids and lipogenic gene expression were analyzed. Additionally, gain-and loss-of-function studies were performed in vitro to identify direct targets of miR-291b-3p. MiR-291b-3p expression and the protein levels of sterol regulatory element-binding protein 1 (SREBP1) and fatty acid synthase (FAS) were increased in the steatotic liver of db/db mice and HFD-fed mice versus their respective controls. Inhibition of hepatic miR-291b-3p expression prevented increases in hepatic lipogenesis and steatosis in HFD-fed mice. The opposite was observed when miR-291b-3p was overexpressed in the livers of chow-fed C57BL/6J wild-type mice. In vitro studies revealed that silencing of miR-291b-3p in NCTC1469 hepatic cells ameliorated oleic acid/palmitic acid mixture-induced elevation of cellular triglycerides. Importantly, we identified AMP-activated protein kinase (AMPK)-␣1 as a direct target of miR-291b-3p. Using metformin, an activator of AMPK, we showed that AMPK activation-induced inhibition of hepatic lipid accumulation was accompanied by reduced expression of miR-291b-3p in the liver. Liver miR-291b-3p promoted hepatic lipogenesis and lipid accumulation in mice. AMPK␣1 is a direct target of miR-291b-3p. In conclusion, our findings indicate that miR-291b-3p promotes hepatic lipogenesis by suppressing AMPK␣1 expression and activity, indicating the therapeutic potential of miR-291b-3p inhibitors in fatty liver disease.

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confidence: 81%

“…Transfection of miRs or siRNA was performed with HiPerFect transfection reagent (Qiagen) as previously described (23).…”

Section: Methodsmentioning

confidence: 99%

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Liver MicroRNA-291b-3p Promotes Hepatic Lipogenesis through Negative Regulation of Adenosine 5′-Monophosphate (AMP)-activated Protein Kinase α1

Meng

Guo

Fang

et al. 2016

Journal of Biological Chemistry

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“…RNA was reversed-transcribed into cDNA using the TaqMan RNA Reverse Transcription kit (Applied Biosystems; Thermo Fisher Scientific, Inc.). qPCR was performed using SYBR Green Supermix (Bio-Rad Laboratories, Inc., Hercules, CA, USA) and the iCycleriQ Real-Time PCR system (Bio-Rad Laboratories, Inc.) as described previously (19). The thermocycling conditons were as followd: at 95˚C for 10 min followed by 50 cycles of 95˚C for 10 sec, 55˚C for 10 sec and 72˚C for 5 sec; 99˚C for 1 sec; 59˚C for 15 sec; 95˚C for 1 sec; then cooling to 40˚C.…”

Section: Rna Extraction and Reverse Transcription-quantitative Polymementioning

confidence: 99%

Nicotinamide N-methyltransferase promotes epithelial-mesenchymal transition in gastric cancer cells by activating transforming growth factor-β1 expression

et al. 2018

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Abstract. Previous studies have demonstrated that nicotinamide N-methyltransferase (NNMT) is aberrantly expressed in a number of tumors. In the present study, it was demonstrated that the gene and protein levels of NNMT were significantly increased in gastric cancer cells. Furthermore, upregulation of NNMT significantly increased the expression of mesenchymal markers, including α-smooth muscle actin (SMA), vimentin and fibronectin, but decreased the levels of epithelial cadherin. Since transforming growth factor (TGF)-β1 may serve a key function in epithelial-mesenchymal transition (EMT), the effects of NNMT on the expression of TGF-β1 were investigated in BGC-823 cells. The results demonstrated that overexpression of NNMT significantly induced the expression of TGF-β1. However, knockdown of NNMT inhibited the expression of TGF-β1, mothers against decapentaplegic homolog (Smad)2 and α-SMA. Additionally, pre-incubation with TGF-β1 partially eliminated NNMT-mediated changes in EMT. Collectively, the results demonstrated that upregulation of NNMT in gastric cancer cells may increase the expression of TGF-β1, therefore activating TGF-β1/Smad signaling, which in turn promotes EMT.

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“…Transfections were performed in 6-, 24-, or 96-well plates after seeded cells were cultured for 24 h. siRNA reagents were transfected using HiPerFect transfection reagent (QIAGEN, Germany) according to the manufacturer's protocol [18]. Briefly, 5 ×10 3 cells/cm 2 were seeded in 200 μL/cm 2 culture.…”

Section: Transfection Of Sirnasmentioning

confidence: 99%

Long Non Coding RNA-UCA1 Contributes to Cardiomyocyte Apoptosis by Suppression of p27 Expression

Liu

Daliang(²,

et al. 2015

Cell Physiol Biochem

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This is an Open Access article licensed under the terms of the Creative Commons AttributionNonCommercial 3.0 Unported license (CC BY-NC) (www.karger.com/OA-license), applicable to the online version of the article only. Distribution permitted for non-commercial purposes only. Key WordsLong non coding RNA • UCA1 • Cardiomyocyte apoptosis • p27 Abstract Background/Aims: Urothelial carcinoma-associated 1 (UCA1) is a recently identified long non coding RNA (lncRNA). However, few studies have explored its role in cardiomyocytes after focal cardiac ischemia reperfusion injury (CIR). Methods: Rat CIR models were established using ligation of the Lower Anterior Descending artery (LAD). Cell apoptosis and reactive oxygen species (ROS) production in cardiac tissues were explored using immunohistochemistry and DHE staining. lncRNA expression patterns were detected using microarray and validated by qPCR. Cell viability and apoptosis were examined using MTT assay and flow cytometry. Results: CIR significantly induced cell apoptosis and ROS production in the rat model. The results of microarray demonstrated the reduced expression of UCA1, which was validated by qPCR. Follow-up experiments showed that UCA1 was involved in H 2 O 2 -induced cell apoptosis. We further showed that UCA1 negatively correlated with the expression of p27. Moreover, overexpression of p27 could induce primary cardiomyocyte apoptosis. Conclusions: Reduction of UCA1 levels plays a pro-apoptotic role in primary cardiomyocytes partially through stimulation of p27 protein expression. These results are in agreement with the observed levels of UCA1, p27 and apoptosis after cardiac I/R injury, suggesting that UCA1 might have an important role during I/R injury.

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MiR-291b-3p Induces Apoptosis in Liver Cell Line NCTC1469 by Reducing the Level of RNA-binding Protein HuR

Cited by 34 publications

References 44 publications

Liver MicroRNA-291b-3p Promotes Hepatic Lipogenesis through Negative Regulation of Adenosine 5′-Monophosphate (AMP)-activated Protein Kinase α1

Liver MicroRNA-291b-3p Promotes Hepatic Lipogenesis through Negative Regulation of Adenosine 5′-Monophosphate (AMP)-activated Protein Kinase α1

Nicotinamide N-methyltransferase promotes epithelial-mesenchymal transition in gastric cancer cells by activating transforming growth factor-β1 expression

Long Non Coding RNA-UCA1 Contributes to Cardiomyocyte Apoptosis by Suppression of p27 Expression

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