Non-coding RNA SNHG1 Research Articles

Nano-Coated si-SNHG14 Regulated PD-L1 Expression and Decreased Epithelial-Mesenchymal Transition in Nasopharyngeal Carcinoma Cells.

To investigate the expression characteristics of long non-coding RNA SNHG14 in nasopharyngeal carcinoma (NPC) and its effects on epithelial-mesenchymal transition and development of nano-coated si-SNHG14 as an anti-tumor agent. The SNHG14 expression in cancerous and adjacent non-cancerous tissues was monitored using reverse transcriptionpolymerase chain reaction (RT-PCR). Gain- and loss-of-function experiments tested the regulation of SNHG14, miR- 5590-3p, and ZEB1 on PD-L1. The binding association between the above three factors was verified using bioinformatics analysis. EMT-related E-cadherin, N-cadherin, and Vimentin were tested using Western blot. Animal experiments in nude mice verified the function of SNHG14 in the EMT of NPC in vivo. The nano-coated si-SNHG14 was developed as an anti-tumor agent and was verified NPC cell in vitro. SNHG14 was upregulated in NPC tissues. Knocking down SNHG14 markedly inhibited the EMT of NPC. Additionally, the expression of ZEB1 was positively related to that of the SNHG14, while it was inversely correlated with that of miR-5590-3p. Moreover, ZEB1 transcription upregulated PD-L1 and promoted the EMT, while SNHG14 could accelerate the EMT of NPC in vivo by regulating the PD-1 and PD-L1. SNHG14-miR-5590- 3p-ZEB1 positively regulated PD-L1 and facilitate the EMT of NPC. Nano-coated si-SNHG14 significantly downregulated PD-L1 expression and decreased EMT.

Silencing of long non-coding RNA SNHG15 suppresses proliferation, migration and invasion of pancreatic cancer cells by regulating the microRNA-345-5p/RAB27B axis.

Pancreatic cancer (PC) is the seventh most common cause of cancer-associated mortality worldwide. The current study aimed to investigate the function and molecular mechanism underlying long non-coding (lnc)RNA SNHG15 in PC tissues and cells. Relative expression levels of lncRNA SNHG15, miR-345-5p and RAB27B in PC cells and tissues were examined by performing reverse transcription-quantitative PCR. The association between SNHG15, miR-345-5p and RAB27B was validated using a Dual-luciferase reporter assay. Proliferation, invasion and migration of PC cells were analysed by conducting MTT, wound healing and Transwell assays. Western blotting was performed to detect the relative expression of the RAB27B protein. The relative expression level of lncRNA SNHG15 and RAB27B was elevated, but that of miR-345-5p was decreased in PC. Silencing of SNHG15 suppressed the proliferation, invasion and migration of PC cells in vitro and suppressed tumour growth in xenograft mice in vivo. miR-345-5p was the target gene of SNHG15 and suppressed cell proliferation, migration and invasion in PC. Furthermore, miR-345-5p targeted RAB27B. The use of miR-345-5p inhibitor or overexpression of RAB27B reversed the suppressive effect of the small interfering RNA si-SNHG15-1 exerted on the proliferation, invasion and migration of PC cells. Silencing of SNHG15 inhibited the proliferation, invasion and migration of PC cells by mediating the miR-345-5p/RAB27B axis, thereby implying its potential as a prognostic marker and target for PC therapy.

LncRNA SNHG15 relieves hyperglycemia-induced endothelial dysfunction via increased ubiquitination of thioredoxin-interacting protein

Numerous studies have revealed that hyperglycemia is a pivotal driver of diabetic vascular complications. However, the mechanisms of hyperglycemia-induced endothelial dysfunction in diabetes remain incompletely understood. This study aims to expound on the underlying mechanism of the endothelial dysfunction induced by hyperglycemia from the perspective of long non-coding RNAs (lncRNA). In this study, a downregulation of SNHG15 was observed in the ischemic hind limb of diabetic mice and high glucose (HG)-treated HUVECs. Functionally, the overexpression of SNHG15 promoted cell proliferation, migration, and tube formation, and suppressed cell apoptosis in HG-treated HUVECs. Mechanistically, SNHG15 reduced thioredoxin-interacting protein (TXNIP) expression by enhancing ITCH-mediated ubiquitination of TXNIP. TXNIP overexpression abrogated the protective effect of lncRNA SNHG15 overexpression on HG-induced endothelial dysfunction. The following experiment further confirmed that SNHG15 overexpression promoted angiogenesis of the ischemic hind limb in diabetic mice. In conclusion, SNHG15 is a novel protector for hyperglycemia-induced endothelial dysfunction via decreasing TXNIP expression.Hyperglycemia is a pivotal driver of vascular complications in diabetes. The present study shows that the long non-coding RNA SNHG15 is downregulated under hyperglycemic conditions. Its overexpression improves hyperglycemia-impaired endothelial dysfunction via reduced expression TXNIP, a thioredoxin-interacting protein. As a novel regulator of endothelial function in diabetes, SNHG15 is a potential therapeutic target for diabetic endothelial dysfunction.

Long Noncoding RNA SNHG7, a Molecular Sponge for microRNA-485, Promotes the Aggressive Behavior of Cervical Cancer by Regulating PAK4 [Retraction

[This retracts the article DOI: 10.2147/OTT.S232542.].

Long Noncoding RNA SNHG16 Silencing Inhibits the Aggressiveness of Gastric Cancer via Upregulation of microRNA-628-3p and Consequent Decrease of NRP1 [Retraction

[This retracts the article DOI: 10.2147/CMAR.S211856.].

Long non-coding RNA SNHG16, binding with miR-106b-5p, promoted cell apoptosis and inflammation in allergic rhinitis by up-regulating leukemia inhibitory factor to activate the JAK1/STAT3 signaling pathway.

Allergic rhinitis (AR) is a type I hypersensitive disease. Long non-coding RNA (lncRNA) SNHG16 acts as an oncogene in a variety of tumors and promotes the occurrence of inflammation in many inflammatory diseases. The study aims to investigate the expression of SNHG16 and its potential biological functions in AR. RT-qPCR results showed that the expression of SNHG16 in AR was up-regulated. The AR cell model was constructed by stimulating primary nasal mucosal epithelial cells from AR patients with IL-13. After knocking down the expression of lncRNA SNHG16, cell apoptosis was detected by flow cytometry, and the expression of inflammatory factors was detected by ELISA. The results showed that SNHG16 promoted cell apoptosis and inflammation. Then, bioinformatics analysis was used to screen miRNAs bound with SNHG16. Luciferase reporter gene assay and RNA pull-down experiment were used to verify the relationship. We found that the expression of miR-106b-5p was down-regulated and leukemia inhibitory factor (LIF) expression was up-regulated in the AR cell model. The expression of phospho-Janus kinase 1 and p-signal transducer and activator of transcription 3 (STAT3) were detected by Western blotting. Silencing the expression of LIF could inhibit the activity of JAK1/STAT3 pathway and further inhibit cell apoptosis and the occurrence of inflammation. Then transfected SNHG16 shRNA alone or together with miR-106b-5p antagomir into the AR cell model, we found that silencing the expression of SNHG16 down-regulated the expression of LIF and inhibited the activity of the JAK1/STAT3 pathway, cell apoptosis, and inflammation. However, miR-106b-5p antagomir weakened its inhibitory effects. The role of SNHG16 in AR was further verified by the ovalbumin-induced AR mouse model in vivo. In conclusion, SNHG16 up-regulates LIF expression by binding with miR-106b-5p, thus promoting the activity of JAK1/STAT3 pathway, and promoting the development of AR. These results provide new targets for the treatment of AR and may help reduce the damage caused by AR.

Long Non-Coding RNA SNHG6 Supports Glioma Progression Through Upregulation of Notch1, Sox2, and EMT.

Gliomas, particularly the advanced grade glioblastomas, have poor 5-year survival rates and worse outcomes. lncRNAs and EMT have been extensively studied in gliomas but the disease progression remains poorly understood. SNHG6 has been shown to affect glioma cell proliferation but its effect on EMT of glioma cells along with its effect on disease progression is not known. We screened four glioma cell lines; H4, A172, U87MG, and SW088 and grouped them based on high vs. low SNHG6 expression. Transfections with SNHG6 specific siRNA resulted in induction of apoptosis of high SNHG6 expressing A172 and U87MG cells. This was accompanied by inhibition of EMT and downregulation of EMT-modulating factor Notch1, β-catenin activity and the cancer stem cell marker Sox2. The regulation was not found to be reciprocal as silencing of Notch1 and Sox2 failed to affect SNHG6 levels. The levels of SNHG6 and Notch1 were also found elevated in Grade IV glioma patients (n = 4) relative to Grade II glioma patients (n = 5). These results identify SNHG6 and Notch1 as valid targets for glioma therapy.

Propofol Protects against Cerebral Ischemia/Reperfusion Injury by Down-Regulating Long Noncoding RNA SNHG14.

Cerebral ischemia-reperfusion (CI/R) injury is a serious central nervous system disease. Propofol (PPF) exerts a neuroprotective effect in CI/R injury; the underlying cause is still unclear. Here, we cultured mouse hippocampal neuron (HT22 cells) in oxygen-glucose deprivation/reoxygenation (OGD/R) conditions to mimic CI/R injury in vitro. PPF treatment promoted cell viability and reduced apoptotic cells in the OGD/R-treated HT22 cells, which was effectively abrogated by SNHG14 overexpression. Moreover, we constructed a CI/R injury mouse model on C57BL/6J mice by middle cerebral artery occlusion/reperfusion (MCAO/R), followed by administration of PPF. PPF reduced neuronal damage and loss, enhanced glial cell hyperplasia, and ameliorated cerebral cortex tissue damage and brain infarct in MCAO/R-induced mice. SNHG14 overexpression aggravated MCAO/R-induced CI/R injury in mice. Furthermore, SNHG14 promoted the expression of Atg5 and Beclin 1 via competitively binding miR-30b-5p, which contributed to activate autophagy and apoptosis in HT22 cells. In addition, the levels of p-p38 and p-SP1 were reduced in the OGD/R-treated HT22 cells in the presence of PPF. SP1 interacted with the promoter of SNHG14 and elevated the expression of SNHG14. PPF treatment inhibited the SP1-mediated up-regulation of SNHG14. In conclusion, this work demonstrates that PPF inhibits SNHG14 expression though the p38 MAPK signaling pathway. SNHG14 promotes Atg5 and Beclin 1 expression by sponging miR-30b-5p and thus activates autophagy and aggravates CI/R injury.

Long noncoding RNA SNHG12 is a potential diagnostic and prognostic biomarker in various tumors

BackgroundTumors 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.MethodsWe 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.ResultsIn 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).ConclusionsOur 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.

Downregulation of long noncoding RNA SNHG7 protects against inflammation and apoptosis in Parkinson's disease model by targeting the miR-425-5p/TRAF5/NF-κB axis.

Accumulated evidence has manifested that long noncoding RNA (lncRNA) is involved in the progress of Parkinson's disease (PD). SNHG7, a novel lncRNA, has been found to be involved in tumorigenesis. However, SNHG7 expression and its functional effects on PD remain uncharted. Rotenone (Rot) was adopted to construct PD models in Sprague-Dawley (SD) rats and SH-SY5Y cells, respectively. The expression levels of caspase 3, tyrosine hydroxylase (TH), ionized calcium-binding adapter molecule 1 (Iba1) in SD rat striatum were measured via immunohistochemistry and western blot. Additionally, the expressions of inflammatory cytokines (interleukin 1β [IL-1β], IL-6, tumor necrosis factor α) and oxidative stress factors (malondialdehyde, superoxide dismutase, and glutathione peroxidase) in the brain tissues were examined using real-time polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. Moreover, the protein levels of tumor necrosis factor receptor-associated factor (TRAF5), I-κB, nuclear factor-κB (NF-κB), HO-1, Nrf2 were detected via western blot. Bioinformatics was applied to predict the targeting relationship between SNHG7, miR-425-5p, and TRAF5. Dual-luciferase activity assay and RNA immunoprecipitation assays were conductedto verify their interactions. In comparison to healthy donors, SNHG7 was found upregulated while miR-425-5p expression was downregulated in PD patients. Functional experiments confirmed that SNHG7 downregulation or miR-425-5p overexpression attenuated neuronal apoptosis in the Rot-mediated PD model, TH-positive cell loss, and microglial activation by mitigating inflammation and oxidative stress. Mechanistically, SNHG7 served as a competitive endogenous RNA by sponging miR-425-5p and promoted TRAF5 mediated inflammation and oxidative stress. Inhibition of SNHG7 ameliorated neuronal apoptosis in PD through relieving miR-425-5p/TRAF5/NF-κB signaling pathway modulated inflammation and oxidative stress, and similar results were observed in the Rot-mediated rat model of PD.

Long non-coding RNA SNHG16 regulates E2F1 expression by sponging miR-20a-5p and aggravating proliferative diabetic retinopathy.

Long non-coding RNAs (lncRNAs) were reported to be related to microvascular dysfunction in diabetic retinopathy (DR), but the potential mechanism remains unknown. This study was designed to elucidate the effects of lncRNA small nucleolar RNA host gene 1 (SNHG16) in proliferative DR progression. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to measure the levels of SNHG16 and miR-20a-5p from peripheral blood samples of different participants. Pearson's correlation analysis was applied to the plasma data to detect correlations between SNHG16 and miR-20a-5p. Finally, the interactions of miR-20a-5p and SNHG16 or E2F1 were assessed by luciferase reporter assays. SNHG16 and E2F1 were increased and miR-20a-5p was decreased in proliferative DR both in vivo and in vitro when compared with control or non-proliferative DR. E2F1 was identified as the target of miR-20a-5p. The miR-20a-5p interacted with SNHG16 and E2F1 and was controlled by SNHG16. The regulation of SNHG16 on E2F1 was mediated by miR-20a-5p. Cells transfected with SNHG16 overexpression plasmid markedly increased cell apoptosis and vessel-like formation, whereas the miR-20a-5p mimic partially reversed these effects. Transfection with gene silencing E2F1 plasmid rescued SNHG16 overexpression-aggravated proliferative DR. This study indicated that SNHG16 regulated E2F1 expression by sponging miR-20a-5p and aggravating proliferative DR.

Long non-coding RNA SNHG1 suppresses cell migration and invasion and upregulates SOCS2 in human gastric carcinoma

Gastric carcinoma (GC) is one of the most common malignancies and the third leading cause of cancer-related deaths worldwide. Long noncoding RNAs (lncRNAs) may be an important class of functional regulators involved in human gastric cancers development. In this study, we investigated the clinical significance and function of lncRNA SNHG1 in GC. SNHG1 was significantly downregulated in GC tumor tissues compared with adjacent noncancerous tissues. Overexpression of SNHG1 in BGC-823 cells remarkably inhibited not only cell proliferation, migration, invasion in vitro, but also tumorigenesis and lung metastasis in the chick embryo chorioallantoic membrane (CAM) assay in vivo. Conversely, inhibition of SNHG1 by transfection of siRNA in AGS cells resulted in opposite phenotype changes. Mechanically, SNHG1 was found interacted with ILF3, NONO and SFPQ. RNA-seq combined with bioinformatic analysis identified a serial of downstream genes of SNHG1, including SOCS2, LOXL2, LTBP3, LTBP4. Overexpression of SNHG1 induced SOCS2 expression whereas knockdown of SNHG1 decreased SOCS2 expression. In addition, knockdown of SNHG1 promoted the activation of JAK2/STAT signaling pathway. Taken together, our data suggested that SNHG1 suppressed aggressive phenotype of GC cells and regulated SOCS2/JAK2/STAT pathway.

RETRACTED ARTICLE: Exosomal SNHG16 secreted by CSCs promotes glioma development via TLR7

BackgroundGlioma is one of the most common central nervous system malignant tumors, accounting for 45~60% of adult intracranial tumors. However, the clinical treatment of glioma is limited. It is of great significance to seek new therapeutic methods for glioma via gene therapy.MethodsLong non-coding RNA (lncRNA) SNHG16 expression level was measured by microarray and qRT-PCR assay; ISH was used to identify the location of SNHG16. Cancer stem cells (CSCs) were separated from glioma tissues and identified using immunofluorescence. Exosomes were isolated from CSCs and cancer cells and identified by TEM and western blot. MTT, wound healing, transwell, and colony formation assay were performed to explore the role of SNHG16 or si-SNHG16 from CSCs on progression of glioma cells. RIP was used to verify the interaction between SNHG16 and TLR7. The experiment of Xenograft used for exploring the function of SNHG16/ TLR7/MyD88/NFκB/c-Myc on growth on glioma in vivo.ResultsMicroarray assay showed long non-coding RNA (lncRNA) SNHG16 was upregulated in glioma. Followed qRT-PCR also showed an increase of SNHG16 in glioma tissues; high expression of SNHG16 indicated a poor prognosis in glioma patients. Interestingly, SNHG16 was packaged into exosomes and derived from CSCs. Functional analysis showed exo-SNHG16 secreted by CSCs promoted the progression of glioma cell lines SHG44 and U251. Furthermore, SNHG16 interacted with TLR7 and activated NFκB/c-Myc signaling in glioma cells. And the silencing of TLR7 inhibited the progression of SHG44 and U251 cells by exo-SNHG16 from CSCs. In vivo tumorigenesis experiments showed that exo-SNHG16 induced glioma progression by activating TLR7/MyD88/NFκB/c-Myc signaling.ConclusionOur study suggested CSC-derived exo-SNHG16 promoted cancer progression by activating TLR7/MyD88/NFκB/c-Myc signaling pathway.

Long Noncoding RNA SNHG12 Promotes Gastric Cancer Proliferation by Binding to HuR and Stabilizing YWHAZ Expression Through the AKT/GSK-3β Pathway.

BackgroundGastric cancer (GC) is a malignancy with high morbidity and mortality rates worldwide. SNHG12 is a long noncoding RNA (lncRNA) commonly involved many types of cancers in the contexts of tumorigenesis, migration and drug resistance. Nevertheless, its role in GC proliferation is poorly understood.MethodsBioinformatics and qRT-PCR assays were used to analyze the expression of SNHG12 in GC tissues and cells. In vitro and in vivo experiments were conducted to detect the role of SNHG12 in GC development. qRT-PCR, PCR, western blotting (WB), RNA binding protein immunoprecipitation (RIP), immunoprecipitation (IP), immunohistochemistry (IHC), fluorescence in situ hybridization (FISH) and in situ hybridization (ISH) were performed to investigate the underlying mechanisms by which SNHG12 promotes GC proliferation.ResultsSNHG12 was highly expressed in GC cells and tissues, and predicted poor survival. In vitro and in vivo assays showed that SNHG12 knockdown inhibited GC proliferation, while SNHG12 overexpression promoted GC proliferation. Further experiments confirmed that SNHG12 was mainly located in the cytoplasm and bound to HuR. Bioinformatics analysis predicted that YWHAZ was the common target of SNHG12 and HuR, and that the “SNHG12-HuR” complex enhanced the stability of YWHAZ mRNA. Furthermore, YWHAZ, which was highly expressed in GC, predicted poor survival and promoted GC proliferation by phosphorylating AKT. Rescue assays verified that SNHG12 promoted GC proliferation by activating the AKT/GSK-3β pathway.ConclusionsSNHG12 binds to HuR and stabilizes YWHAZ. SNHG12 promotes GC proliferation via modulation of the YWHAZ/AKT/GSK-3β axis in vitro and in vivo. Thus, SNHG12 could become a novel therapeutic target for anti-tumor therapy.

Retraction.

Retraction: "Long noncoding RNA SNHG16 contributes to the development of bladder cancer via regulating miR-98/STAT3/Wnt/β-catenin pathway axis," by Feng Feng, Aiping Chen, Junjian Huang, Qinghua Xia, Yougen Chen, Xunbo Jin, J Cell Biochem. 2018; 9408-9418: The above article, published online on 21 August 2018 in Wiley Online Library (https://onlinelibrary.wiley.com/doi/abs/10.1002/jcb.27257), has been retracted by agreement between the journal's Editor in Chief, Prof. Dr. Christian Behl, and Wiley Periodicals LLC. The retraction has been agreed following an investigation based on allegations raised by a third party. Several flaws and inconsistencies between results presented and experimental methods described were found, the editors consider the conclusions of this article to be invalid. The authors collaborated in the investigation initially, but were not available for a final confirmation of the retraction.

Long non-coding RNA SNHG16 contributes to progression of carotid atherosclerosis by regulating miR-30c-5p/ADAM10 axis

IntroductionCarotid atherosclerosis (CAS) is one of the main causes of cerebral infarction in the ageing population. Long non-coding RNA small nucleolar RNA host gene 16 (lnc-SNHG16) could promote the development of atherosclerosis. However, the mechanism of lnc-SNHG16 in CAS remains vague.Material and methodsThe expression levels of lnc-SNHG16, microRNA-30c-5p (miR-30c-5p) and disintegrin and metalloproteinase 10 (ADAM10) were detected by real-time quantitative polymerase chain reaction (RT-qPCR). Cell viability and migration were detected by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) and transwell assays, severally. The levels of interleukin-6 (IL-6), IL-β and tumor necrosis factor-α (TNF-α) were assessed by enzyme-linked immunosorbent assay (ELISA). Protein levels of spinal muscular atrophy (SMA), calponin and ADAM10 were examined by western blot assay. The binding relationship between miR-30c-5p and lnc-SNHG16 or ADAM10 was predicted by Starbase, then verified by the dual-luciferase reporter assay.ResultsLnc-SNHG16 and ADAM10 were increased, and miR-30c-5p was decreased in CAS patient and oxidized low-density lipoprotein (ox-LDL)-treated human aortic smooth muscle cells (hASMCs). Lnc-SNHG16 silencing repressed cell viability, migration, inflammation, facilitated differentiation in ox-LDL-treated hASMCs. Moreover, mechanical analysis proved that lnc-SNHG16 improved ADAM10 expression by sponging miR-30c-5p.ConclusionsOur data indicated that lnc-SNHG16 could regulate the progression of ox-LDL induced CAS model by the miR-30c-5p/ADAM10 axis, implying a potential therapeutic strategy for CAS

Long non-coding RNA SNHG1 mediates neuronal damage in Parkinson's disease model cells by regulating miR-216a-3p/Bcl-2-associated X protein.

BackgroundParkinson’s disease (PD) is a common central nervous system degenerative disease in middle-aged and elderly people. Our study aimed to illuminate the relationship and mechanism of long-chain non-coding RNA SNHG1 and miRNA (miR)-216a-3p in PD.MethodsHuman neuroblastoma cell lines were treated with MPP+ to construct a PD model. Real-time fluorescent quantitative PCR was used to detect the cellular expression of SNHG1. Neuronal cell activity and apoptosis were compared before and after SNHG1 knock-down, as was neuronal miR-216a-3p expression. Further, a luciferase reporter gene experiment was performed to verify BAX as the target of miR-216a-3p. Anti-miR-216a-3p and BAX were co-transfected into PD model cells, and neuronal cellular activity and apoptosis were observed. Finally, the potential regulatory network of SNHG1/miR-216a-3p/BAX in PD was investigated.ResultsThe expression of miR-216a-3p was decreased in the PD model cells, and re-expression reversed the high apoptotic rate and cell vitality inhibition in PD model cells. SNHG1 interacted with miR-216a-3p and negatively regulated its upstream molecules, while miR-216a-3p attenuated the effect of SNHG1 knock-down on neurons. The overexpression of BAX in the PD cell model blocked the damage by miR-216a-3p to neurons. At the same time, SNHG1 acted as a coordinator, mediating the regulation of BAX via miR-216a-3p, thereby affecting the activity and apoptotic rate of neurons in the PD model.ConclusionsSNHG1 interacts with miR-216a-3p to regulate the expression of BAX. This SNHG1/miR-216a-3p/BAX molecular regulatory network is implicated in the pathogenesis of PD.

Clinicopathological and prognostic value of long noncoding RNA SNHG7 in cancer patients: a meta-analysis.

Recent studies have provided evidence that long noncoding RNA SNHG7 is highly expressed and associated with poor clinical outcomes in cancer patients. The meta-analysis is aimed to evaluate the prognostic value of SNHG7 across various cancers. Eligible studies about prognosis and clinicopathological features of SNHG7 expression in all kinds of tumors were collected by searching the databases of PubMed, Web of Science, Embase, Cochrane Library from inception through August 13, 2020. Odds ratios (ORs) and hazard ratios (HRs) with 95% confidence intervals (CIs) from eligible studies were extracted and pooled to investigate the association between SNHG7 and survival or clinicopathology by STATA 16.0 software. A total of 13 studies enrolling 1029 cancer patients met the inclusion criteria in this meta-analysis. Based on the results, over-expressed SNHG7 was associated with deeper tumor invasion (OR: 2.76; 95% CI: 1.98-3.86; p: 0.000), earlier lymphatic metastasis (OR: 4.22; 95% CI: 3.04-5.86; p: 0.000), more advanced tumor stage (OR: 3.49; 95% CI: 2.45-4.98; p: 0.000) and poor histologic grade (OR: 2.23; 95% CI: 1.33-3.74; p: 0.002), but not with sex, age, tumor size and distant metastasis. As for prognosis, patients with high expression of SNHG7 were more likely to have shorter overall survival (OS) (HR: 1.64; 95% CI: 1.38-1.94; p: 0.000) and disease-free survival (DFS) (HR: 1.37; 95% CI: 1.09-1.71; p: 0.006). SNHG7 may serve as a novel biomarker in terms of predicting prognosis and clinicopathological characters in various human cancers.

Long non-coding RNA SNHG14 aggravates LPS-induced acute kidney injury through regulating miR-495-3p/HIPK1.

Acute kidney injury (AKI) is a complex syndrome with an abrupt decrease of kidney function, which is associated with high morbidity and mortality. Sepsis is the common cause of AKI. Mounting evidence has demonstrated that long non-coding RNAs (lncRNAs) play critical roles in the development and progression of sepsis-induced AKI. In this study, we aimed to illustrate the function and mechanism of lncRNA SNHG14 in lipopolysaccharide (LPS)-induced AKI. We found that SNHG14 was highly expressed in the plasma of sepsis patients with AKI. SNHG14 inhibited cell proliferation and autophagy and promoted cell apoptosis and inflammatory cytokine production in LPS-stimulated HK-2 cells. Functionally, SNHG14 acted as a competing endogenous RNA (ceRNA) to negatively regulate miR-495-3p expression in HK-2 cells. Furthermore, we identified that HIPK1 is a direct target of miR-495-3p in HK-2 cells. We also revealed that the SNHG14/miR-495-3p/HIPK1 interaction network regulated HK-2 cell proliferation, apoptosis, autophagy, and inflammatory cytokine production upon LPS stimulation. In addition, we demonstrated that the SNHG14/miR-495-3p/HIPK1 interaction network regulated the production of inflammatory cytokines (TNF-α, IL-6, and IL-1β) via modulating NF-κB/p65 signaling in LPS-challenged HK-2 cells. In conclusion, our findings suggested a novel therapeutic axis of SNHG14/miR-495-3p/HIPK1 to treat sepsis-induced AKI.

LncRNA SNHG1 protects the cardiac muscle cells from hypoxia/ re-oxygenation injury in vitro by targeting microRNA-21-5p and miR-30a-5p

Purpose: Cardiovascular diseases are responsible for numerous deaths globally. Long noncoding RNA SNHG1 has presented its protective role in cardiomyocytes previously. Herein, we examined the underlying molecular mechanisms of SNHG1 in cardiac muscle cells from hypoxia and re-oxygenation (H/R) in vitro.Methods: RT-qPCR measured expression of SNHG1, miR-21-5p and miR-30a-5p in rat cardiac muscle cell line HL-1 before and after H/R treatment and cell transfection, which was applied to regulate expression of SNHG1, miR-21-5p and miR-30a-5p for further use. The flow cytometry method was used to compare changes in cellular apoptosis, and cell viability was measured by CCK-8 method.Bioinformatics predicted the bindings ofSNHG1 and miR-21-5p / miR-30a-5p while the luciferase reporter assays further verified this.Results: The outcomes revealedthat SNHG1 was downregulated and meanwhile miR-21-5p / miR-30a5p was elevated that enhanced apoptosis and reduced cell viability in HL-1 cells. However, overexpressed SNHG1 inhibited cell apoptosis and increased cell viability brought by H/R. In addition, SNHG1 targeted at miR-21-5p/ miR-30a-5p, which contributed to the inter-regulation in between. Furthermore, interactive experiments revealed that upregulation of miR-21-5p/ miR-30a-5p added to the cell apoptosis which was induced by H/R and partially counteracted by the upregulation of SNHG1.Conclusion: In this study we have demonstrated the protective role of SNHG1 in the moderation of H/R-induced HL-1 apoptosis and viability through suppression of miR-21-5p/miR-30a-5p. This offers new perspective into the molecular interpretation of cardiovascular diseases such as ischemic reperfusion injury.&#x0D; Keywords: SNHG1; apoptosis; Hypoxia/Re-oxygenation injury;miR-21-5p; miR-30a-5p; Cardiovascular diseases