LncRNA SNHG12 inhibits miR-199a to upregulate SIRT1 to attenuate cerebral ischemia/reperfusion injury through activating AMPK signaling pathway

Yin, Wei-Lan; Yin, Wen; Huang, Biao; Wu, Lixiang

doi:10.1016/j.neulet.2018.08.026

Cited by 59 publications

(39 citation statements)

References 29 publications

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“…Recently, increasing studies have discovered the underlying mechanisms of long noncoding RNAs at multiple regulatory levels 32 . For SNHG12, almost all existing studies agreed that it works as a miRNA sponge in different cancer cells 16 , 18 , 33 , 34 . By this mechanism, SNHG12 functions as an endogenous competitive mimic target of miRNAs, which results in the upregulation of the mRNA that is regulated by these miRNAs.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA SNHG12 promotes tumour progression and sunitinib resistance by upregulating CDCA3 in renal cell carcinoma

et al. 2020

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Renal cell carcinoma (RCC) is one of the most frequently observed malignant tumours in the urinary system and targeted drug resistance is quite common in RCC. Long noncoding RNA SNHG12 (lncRNA SNHG12) has emerged as a key molecule in numerous human cancers, but its functions in renal cell carcinoma (RCC) sunitinib resistance remain unclear. In this study, we found SNHG12 was highly expressed in RCC tissues and in sunitinib-resistant RCC cells and was associated with a poor clinical prognosis. SNHG12 promoted RCC proliferation, migration, invasion and sunitinib resistance via CDCA3 in vitro. Mechanically, SNHG12 bound to SP1 and prevented the ubiquitylation-dependent proteolysis of SP1. Stabilised SP1 bound to a specific region in the promoter of CDCA3 and increased CDCA3 expression. Furthermore, in vivo experiments showed that SNHG12 increased tumour growth and that knocking down SNHG12 could reverse RCC sunitinib resistance. Our study revealed that the lncRNA SNHG12/SP1/CDCA3 axis promoted RCC progression and sunitinib resistance, which could provide a new therapeutic target for sunitinib-resistant RCC.

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Section: Discussionmentioning

confidence: 99%

Long noncoding RNA SNHG12 promotes tumour progression and sunitinib resistance by upregulating CDCA3 in renal cell carcinoma

et al. 2020

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“…SNHG12 is negative regulation miR-195-5p, miR-320, miR-129, miR-193a-3p, microRNA-199a/b-5p and miR-424-5 [11,14,15,17,26] . Yin, Zhao and Long found that SNHG12 regulates brain microvascular endothelial cell death, the in ammatory response, and angiogenesis during and after ischemic stroke through target genes and signaling pathways (Sirt1, AMPK signaling pathway, and miR-150/VEGF pathway) [38][39][40] . In addition, the expression level of SNHG12 in gastric cancer, osteoma, colon cancer, hepatocellular carcinoma and various other tumors is related to the clinical features and prognosis of cancer patients.…”

Section: Discussionmentioning

confidence: 99%

Long Noncoding RNA SNHG12 is a Potential Diagnostic and Prognostic Biomarker in Various Tumors

Wang

Jiang

Zhang³

et al. 2020

Preprint

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Background. Tumors are the second most common cause of death in humans worldwide, second only to cardiovascular and cerebrovascular diseases. Although methods and techniques for the treatment of tumors continue to improve, the effect is not satisfactory. These may lack effective therapeutic targets. This study aimed to evaluate the value of SNHG12 as a biomarker in the prognosis and clinical characteristics of various cancer patients.Methods. We analyzed SNHG12 expression and plotted the survival curves of all cancer samples in the TCGA database using the GEPIA tool. Then, we searched for eligible papers up to April 1, 2019 in databases. Next, the data were extracted from studies examining SNHG12 expression, overall survival and clinicopathological features in patients with malignant tumors. We used Review Manager 5.3 and Stata 15 software to analyze the statistical data.Results. In the TCGA database, abnormally high expression of SNHG12 in tumor samples indicates that the patient has a poor prognosis. Results of meta-analysis is that SNHG12 high expression is related to low overall survival (HR=2.72, 95% CI=1.95-3.8, P<0.00001), high tumor stage (OR=3.94, 95% CI=2.80-5.53, P<0.00001), high grade (OR=2.04, 95% CI=1.18-3.51, P=0.01), distant metastasis (OR=2.20, 95% CI=1.40-3.46, P=0.0006), tumor size (OR=2.79, 95% CI=1.89-4.14, P<0.00001) and lymph node metastasis (OR=2.66, 95%CI=1.65-4.29, P<0.0001).Conclusions. Our study confirmed that the high expression level of SNHG12 is closely related to the clinicopathological characteristics and prognosis of patients and is a new predictive biomarker for various cancer patients.

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“…Previous studies have shown that the lncRNA N1LR exerts a neuroprotective effect against ischemic stroke by inhibiting p53 phosphorylation. The lncRNA SNHG12 inhibits miR-199a to upregulate SIRT1 and attenuates cerebral I/R injury by activating the AMPK signaling pathway [30]. The lncRNA MEG3 functions as a competing endogenous RNA to regulate ischemic neuronal death by targeting the miR-21/PDCD4 signaling pathway [11].…”

Section: Discussionmentioning

confidence: 99%

Overexpression of the long non-coding RNA Oprm1 alleviates apoptosis from cerebral ischemia-reperfusion injury through the Oprm1/miR-155/GATA3 axis

Jing

Liu

Jia

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Numerous differentially expressed long non-coding RNAs (lncRNAs) have been identified in cerebral ischemia-reperfusion (I/R) injury using RNA-Seq analysis. However, little is known about whether and how lncRNAs are involved in cerebral I/R injury. In this study, we investigated the function of the lncRNA Oprm1 in cerebral I/R injury and explored the underlying mechanism. An oxygen-glucose deprivation model in N2a cells was utilized to mimic cerebral I/R injury in vitro. Trypan blue staining, terminal deoxytransferase-mediated dUTP-biotin nick end labelling and caspase-3 were measured to evaluate apoptosis. Middle cerebral artery occlusion was performed in mice to evaluate the function of lncRNA Oprm1 in vivo. Real-time PCR and western blotting were used to measure the expression levels of lncRNA Opmr1, caspase-3, miR-155, GATA binding protein 3 (GATA3) and nuclear factor (NF)-jB. lncRNA Oprm1 was mainly located in the cytoplasm. Overexpression of lncRNA Oprm1 alleviated the apoptosis induced by oxygen-glucose deprivation and significantly reduced cleaved caspase-3 levels. Infarct size was distinctly decreased in the lncRNA Oprm1-overexpression group. The neurological score was also improved. Our findings showed that the lncRNA Oprm1/miR-155/GATA3 axis plays an important role in cerebral I/R injury. lncRNA Oprm1 may attenuate cerebral injury through the NF-jB pathway. lncRNA Oprm1 may serve as a potential target for new therapeutic interventions in patients with ischemic stroke. ARTICLE HISTORY

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LncRNA SNHG12 inhibits miR-199a to upregulate SIRT1 to attenuate cerebral ischemia/reperfusion injury through activating AMPK signaling pathway

Cited by 59 publications

References 29 publications

Long noncoding RNA SNHG12 promotes tumour progression and sunitinib resistance by upregulating CDCA3 in renal cell carcinoma

Long noncoding RNA SNHG12 promotes tumour progression and sunitinib resistance by upregulating CDCA3 in renal cell carcinoma

Long Noncoding RNA SNHG12 is a Potential Diagnostic and Prognostic Biomarker in Various Tumors

Overexpression of the long non-coding RNA Oprm1 alleviates apoptosis from cerebral ischemia-reperfusion injury through the Oprm1/miR-155/GATA3 axis

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