lncRNA SNHG1 Research Articles

SPATS2 is positively activated by long noncoding RNA SNHG5 via regulating DNMT3a expression to promote hepatocellular carcinoma progression.

Hepatocellular carcinoma (HCC) is one of the most prevalent malignant tumors with high mortality worldwide. Spermatogenesis-associated serine-rich 2 (SPATS2) could be a novel diagnostic and prognostic biomarker in HCC. However, the regulatory mechanism of SPATS2 in HCC requires further elucidation. Therefore, the study’s objective was to investigate this process in HCC. In this study, we found that SPATS2 is significantly upregulated in HepG2 cells to promote cell growth and migration. SPATS2 is the target transcript of lncRNA SNHG5. SPATS2 positively affects the proliferation and migration of HepG2 cells caused by the higher expression of SNHG5. Mechanistically, we identified that the elevated of SPATS2 was attributed to SNHG5 related hypomethylation of SPATS2. SNHG5 reduced the expression of DNMT3a to suppress the methylation level of SPATS2. Taken together, our results uncover a novel epigenetic regulatory mechanism of lncRNA SNHG5-DNMT3a axis-related SPATS2 expression underlying HCC progression. This may serve as a novel prognostic marker and a promising therapeutic target for the treatment of HCC.

LncRNA SNHG3 regulates the BMSC osteogenic differentiation in bone metastasis of breast cancer by modulating the miR-1273g-3p/BMP3 axis

BackgroundResearch on the role of lncRNAs in the process of bone metastasis in breast cancer (BM-BCa) has just begun at an early stage, and an increasing number of lncRNAs have been proved to play a regulatory role in the process of BM-BCa. Our study focused on the balance of osteogenic-osteoclast regulated by lncRNA-SNHG3 in bone metastasis microenvironment. MethodsSNHG3 level of clinical tissues and breast cancer cell lines was determined by RT-qPCR. ALP staining, ALP activity identification and western blotting of OPG, OSX, RUNX2, BMP2 together with BMP3 was performed to verify the osteogenesis of bone marrow mesenchymal stem cells (BMSCs) both in vitro and in vivo. Exosomes derived from MDA-MB-231 were characterized and sequenced, followed by RT-qPCR. Dual luciferase reporter gene assay was utilized to analyze the binding sites of miR-1273g-3p on SNHG3 and BMP3. ResultsExpression of BMP3 was positively regulated by SNHG3 via exosomal miR-1273g-3p. ConclusionThe overexpression of SNHG3 in breast cancer cells may be responsible for osteolytic metastasis Thus, knockdown of SNHG3 might be a potential target for improvement of BM-BCa Treatment.

LncRNA SNHG15 Induced by SOX12 Promotes the Tumorigenic Properties and Chemoresistance in Cervical Cancer via the miR-4735-3p/HIF1a Pathway.

Cervical cancer (CC) is one of the most common malignancies in females, with high prevalence and mortality globally. Despite advances in diagnosis and therapeutic strategies developed in recent years, CC is still a major health burden worldwide. The molecular mechanisms underlying the development of CC need to be understood. In this study, we aimed to demonstrate the role of lncRNA SNHG15 in CC progression. Using qRT-PCR, we determined that lncRNA SNHG15 is highly expressed in CC tumor tissues and cells. lncRNA SNHG15 knockdown also reduces the tumorigenic properties of CC in vitro, as determined using the MTT, EdU, flow cytometry, and transwell assays. Using bioinformatics analysis, RNA pull-down, ChIP, and luciferase reporter assays, we verified the molecular mechanisms of lncRNA SNHG15 in CC progression and found that lncRNA SNHG15 expression in CC cells is transcriptionally regulated by SOX12; moreover, lncRNA SNHG15 promotes CC progression via the miR-4735-3p/HIF1a axis. This study can provide a potential target for CC diagnosis or therapeutic strategies in the future.

Prenatal Cadmium Exposure Alters Proliferation in Mouse CD4+ T Cells via LncRNA Snhg7.

ObjectivePrenatal cadmium (Cd) exposure leads to immunotoxic phenotypes in the offspring affecting coding and non-coding genes. Recent studies have shown that long non-coding RNAs (lncRNAs) are integral to T cell regulation. Here, we investigated the role of long non-coding RNA small nucleolar RNA host gene 7 (lncSnhg7) in T cell proliferation.MethodsRNA sequencing was used to analyze the expression of lncRNAs in splenic CD4+ T cells with and without CD3/CD28 stimulation. Next, T cells isolated from offspring exposed to control or Cd water throughout mating and gestation were analyzed with and without stimulation with anti-CD3/CD28 beads. Quantitative qPCR and western blotting were used to detect RNA and protein levels of specific genes. Overexpression of a miR-34a mimic was achieved using nucleofection. Apoptosis was measured using flow cytometry and luminescence assays. Flow cytometry was also used to measure T cell proliferation in culture. Finally, lncSnhg7 was knocked down in splenic CD4+ T cells with lentivirus to assess its effect on proliferation.ResultsWe identified 23 lncRNAs that were differentially expressed in stimulated versus unstimulated T cells, including lncSnhg7. LncSnhg7 and a downstream protein, GALNT7, are upregulated in T cells from offspring exposed to Cd during gestation. Overexpression of miR-34a, a regulator of lncSnhg7 and GALNT7, suppresses GALNT7 protein levels in primary T cells, but not in a mouse T lymphocyte cell line. The T cells isolated from Cd-exposed offspring exhibit increased proliferation after activation in vitro, but Treg suppression and CD4+ T cell apoptosis are not affected by prenatal Cd exposure. Knockdown on lncSnhg7 inhibits proliferation of CD4+ T cells.ConclusionPrenatal Cd exposure alters the expression of lncRNAs during T cell activation. The induction of lncSnhg7 is enhanced in splenic T cells from Cd offspring resulting in the upregulation of GALNT7 protein and increased proliferation following activation. miR-34a overexpression decreased GALNT7 expression and knockdown of lncSnhg7 inhibited proliferation suggesting that the lncSnhg7/miR-34a/GALNT7 is an important pathway in primary CD4+ T cells. These data highlight the need to understand the consequences of environmental exposures on lncRNA functions in non-cancerous cells as well as the effects in utero.

LncRNA SNHG14 promoted inflammation of cerebral apoplexy by miR-124-3p/TRAF6 axis

LncRNA SNHG14 promoted inflammation of cerebral apoplexy by miR-124-3p/TRAF6 axis

Retracted] lncRNA SNHG3 promotes breast cancer progression by acting as a miR‑326 sponge.

Following the publication of the above article, the authors have requested that it be retracted. Subsequently to having performed these experiments, the authors have realized that their MCF‑7 cells had become contaminated while performing the colony formation and transwell experiments. Furthermore, they were unable to reproduce the results from the invivo experiments, and knockdown of SNHG3 was found not to affect tumor growth in nude mice. Following a further investigation in the Editorial Office, it also came to light that there were other possible anomalies associated with the presentation of the tumor images in Fig.6B and the colony formation assay data in Fig.2C. Therefore, theos article has been retracted from the Journal; all the authors agree to this retraction. The Editor and the authors would like to apologize for any inconvenience caused. [the original article was published in Oncology Reports 44: 1502‑1510, 2020; DOI: 10.3892/or.2020.7690].

Prognostic effect of lncRNA SNHG7 on cancer outcome: a meta and bioinformatic analysis

BackgroundNew evidence from clinical and fundamental researches suggests that SNHG7 is involved in the occurrence and development of carcinomas. And the increased levels of SNHG7 are associated with poor prognosis in various kinds of tumors. However, the small sample size was the limitation for the prognostic value of SNHG7 in clinical application. The aim of the present meta-analysis was to conduct a qualitative analysis to explore the prognostic value of SNHG7 in various cancers.MethodsArticles related to the SNHG7 as a prognostic biomarker for cancer patients, were comprehensive searched in several electronic databases. The enrolled articles were qualified via the preferred reporting items for systematic reviews and meta-analysis of observational studies in epidemiology checklists. Additionally, an online database based on The Cancer Genome Atlas (TCGA) was further used to validate our results.ResultsWe analyzed 2418 cancer patients that met the specified criteria. The present research indicated that an elevated SNHG7 expression level was significantly associated with unfavorable overall survival (OS) (HR = 2.45, 95% CI: 2.12–2.85, p <0.001). Subgroup analysis showed that high expression levels of SNHG7 were also significantly associated with unfavorable OS in digestive system cancer (HR = 2.31, 95% CI: 1.90–2.80, p <0.001) and non-digestive system cancer (HR = 2.67, 95% CI: 2.12–3.37, p <0.001). Additionally, increased SNHG7 expression was found to be associated with tumor stage and progression (III/IV vs. I/II: HR = 1.76, 95% CI: 1.57–1.98, p <0.001). Furthermore, elevated SNHG7 expression significantly predicted lymph node metastasis (LNM) (HR = 1.98, 95% CI: 1.74–2.26, p <0.001) and distant metastasis (DM) (HR = 2.49, 95% CI: 1.88–3.30, p <0.001) respectively. No significant heterogeneity was observed among these studies. SNHG7 was significantly upregulated in four cancers and the elevated expression of SNHG7 predicted shorter OS in four cancers, worse DFS in five malignancies and worse PFI in five carcinomas based on the validation using the GEPIA on-line analysis tool.ConclusionsThe present analysis suggests that elevated SNHG7 is significantly associated with unfavorable OS, tumor progression, LNM and DM in various carcinomas, and may be served as a promising biomarker to guide therapy for cancer patients.

LncRNA SNHG12 Promotes Osteoarthritis Progression Through Targeted Down-Regulation of miR-16-5p.

In accordance with increasing studies, long non-coding RNAs (LncRNAs) act pivotally in the occurrence as well as development of several human diseases. But how lncRNA SNHG12 acts in osteoarthritis (OA) is still not clear. We applied CCK-8 to determine cell viability, along with qRT-PCR to detect mRNA expression. Using luciferase reporter experiment, our team detected the binding relationship between lncRNA SNHG12 along with miR-16-5p. The inflammatory factor IL-1β induced chondrocytes to express lncRNA SNHG12, and lncRNA SNHG12 expression was up-regulated in OA tissues. Additionally, our personnel proved that IL-1β inhibited miR-16-5p expression in chondrocytes, which in OA tissues was lower than that in normal tissues. miR-16-5p expression level in the OA patients' tissue was negatively correlated with lncRNA SNHG12 expression. The high-expression lncRNA SNHG12 inhibits chondrocyte proliferation, promoting apoptosis and inflammation as well as extracellular matrix (ECM) degradation. These effects can be reversed by co-transfecting miR-16-5p mimic. In addition, our work revealed that miR-16-5p is a target of lncRNA SNHG12. lncRNA SNHG12 regulates OA development by inhibiting miR-16-5p expression in chondrocytes. We believe that the lncRNA SNHG12/miR-16-5p axis might be a potential therapeutic and diagnostic target for OA.

LncRNA SNHG5 can Regulate the Proliferation and Migration of Diffuse Large B Cell Lymphoma Progression via Targeting miR-181-5p/XIAP.

Background: It has been verified that long noncoding RNAs (lncRNAs) may participate in the pathogenesis of various human diseases. This study aims to investigate the roles of lncRNA SNHG5 in diffuse large B cell lymphoma (DLBC), especially the impacts of lncRNA SNHG5 on proliferation and migration of human diffuse large B cell lymphoma cells and the related mechanism.Methods: qRT-PCR analysis was carried out to examine the expression pattern of SNHG5 in DLBC tissue and adjacent normal tissue. The effect of SNHG5 on the proliferation, apoptosis, migration, and invasion of DLBC cells was detected by MTT, flow cytometry analysis, wound healing assay and transwell assay. The correlation between SNHG5, miR-181-5p and XIAP were certified by bioinformatics analysis, and dual-luciferase reporter assay. Furthermore, rescue assays were performed to analyze the effects of SNHG5-miR-181-5p-XIAP axis on the biological behaviors of diffuse large B cell lymphoma cells. Finally, the effects of SNHG5 axis on the growth of DLBC tumor was examined by in vivo analysis.Results: SNHG5 was significantly upregulated in diffuse large B cell lymphoma tissues. Knockdown of SNHG5 inhibited the proliferation, migration, and invasion of diffuse large B cell lymphoma cells in vitro and in vivo. LncRNA SNHG5 acted as a ceRNA through binding with miR-181-5p in DLBC cells.Conclusion: LncRNA SNHG5 may promote proliferation and migration of diffuse large B cell lymphoma cells via targeting miR-181-5p/XIAP.

Biomarkers associated with metastasis and prognosis of lung adenocarcinoma based on microarray data.

We attempted to discover the biomarker associated with metastasis and prognosis of lung adenocarcinoma. The mRNA/lncRNA expression profiles (GSE101836) were downloaded from the publicly available database, which included three highly metastatic and three weakly metastatic samples. The differentially expressed genes and lncRNAs were analyzed and survival analysis were performed based on the TCGA database. The prognosis-associated PPI network and mRNA-lncRNA coexpression network were constructed followed by the function and pathway enrichment analysis. The expression levels of key genes were validated in other datasets. Difference in gender was analyzed. Total 256 differentially expressed genes and 2 lncRNAs were found to be closely related with prognosis. PPI network was constructed with 222 nodes and 1464 edges. Two modules were divided from PPI network. Genes in module A were significantly enriched in cell cycle checkpoint, chromosome segregation, and mitotic cell cycle checkpoint. The module B was closely related with pyridine nucleotide metabolic process, nicotinamide nucleotide metabolic process and carbon metabolism. Coexpression network revealed lncRNA H19 and lncRNA SNHG12 were significant nodes. SNHG12 was closely related with GO:0006260~DNA replication, GO:0055114~oxidation-reduction process and hsa00010: Glycolysis/Gluconeogenesis. H19 was enriched in GO:0006555~methionine metabolic process, and GO:0046655~folic acid metabolic process. The expression levels of TTK and CCNB1 were confirmed in other datasets. The expression of TTK and CCNB1 was significantly higher in the male group than in the female group. TTK, CCNB1 and lncRNA SNHG12 may be the biomarker associated with metastasis and prognosis of lung adenocarcinoma.

Regulatory Effects of LncRNA SNHG4 on miR-25/FBXW7 Axis in Papillary Thyroid Cancer Cells.

We analyzed the interaction between miR-25 and SNHG4 in papillary thyroid cancer (PTC). LncRNA SNHG4 was identified as an oncogene in osteosarcoma. We analyzed The Cancer Genome Atlas (TCGA) data and found that SNHG4 was downregulated in papillary thyroid cancer (PTC). Sixty patients with PTC were enrolled. SNHG4 expression in paired PTC tissues and adjacent normal tissues from the 60 PTC patients was analyzed by reverse transcription quantitative polymerase chain reaction. The proliferation of IHH-4 cells with SNHG4, miR-25 or FBXW7 overexpression was analyzed by cell proliferation assay. SNHG4 was downregulated in PTC tissues compared with the adjacent normal tissues of PTC patients. SNHG4 sponged with miR-25, while SNHG4 and miR-25 overexpression failed to alter each other. SNHG4 overexpression resulted in upregulated FBXW7, which is a targeted of miR-25. miR-25 overexpression increased PTC cell proliferation. Overexpression of SNHG4 and FBXW7 played an opposite role and abolished the effect of miR-25 overexpression. SNHG4 may interact with the miR-25/FBXW7 axis to suppress PTC cell proliferation.

LncRNA Snhg5 Attenuates Status Epilepticus Induced Inflammation through Regulating NF-κΒ Signaling Pathway.

Status epilepticus (SE) induced inflammation plays an important role in the pathogenesis of SE. Long non-coding RNA small nucleolar RNA host gene 5 (lncRNA Snhg5) has been reported in various inflammatory diseases. However, the mechanism of Snhg5 regulated inflammation in SE remains unclear. Therefore, this study aimed to clarify the role and mechanism of Snhg5 in SE-induced inflammation in vitro and vivo. In vitro, lipopolysaccharide (LPS)-induced inflammation in microglia was used to mimic the inflammation after SE. In vivo, SE model was induced by lithium chloride and pilocarpine. The level of Snhg5, p65, p-p65, p-inhibitor of kappaB (IκB)α, IκBα and inflammatory factors (tumor necrosis factor (TNF)-α, interleukin (IL)-1β) were measured via quantitative real-time PCR or Western blot. The Nissl stain and immunohistochemical stain were performed to observe hippocampal damage and microglia proliferation. The results showed Snhg5 was up-regulated in the rat and microglia. Knockdown of Snhg5 inhibited LPS-induced inflammation and relative expression of p-65/p65, p-IκBα/IκBα. Moreover, down-regulation of Snhg5 attenuated SE-induced inflammation and reduced the number of microglia in hippocampus. These findings indicated that Snhg5 modulates the inflammation via nuclear factor-kappaB (NF-κB) signaling pathway in SE rats.

A comprehensive analysis of ncRNA-mediated interactions reveals potential prognostic biomarkers in prostate adenocarcinoma

As one of common malignancies, prostate adenocarcinoma (PRAD) has been a growing health problem and a leading cause of cancer-related death. To obtain expression and functional relevant RNAs, we firstly screened candidate hub mRNAs and characterized their associations with cancer. Eight deregulated genes were identified and used to build a risk model (AUC was 0.972 at 10 years) that may be a specific biomarker for cancer prognosis. Then, relevant miRNAs and lncRNAs were screened, and the constructed primarily interaction networks showed the potential cross-talks among diverse RNAs. IsomiR landscapes were surveyed to understand the detailed isomiRs in relevant homologous miRNA loci, which largely enriched RNA interaction network due to diversities of sequence and expression. We finally characterized TK1, miR-222-3p and SNHG3 as crucial RNAs, and the abnormal expression patterns of them were correlated with poor survival outcomes. TK1 was found synthetic lethal interactions with other genes, implicating potential therapeutic target in precision medicine. LncRNA SNHG3 can sponge miR-222-3p to perturb RNA regulatory network and TK1 expression. These results demonstrate that TK1:miR-222-3p:SNHG3 axis may be a potential prognostic biomarker, which will contribute to further understanding cancer pathophysiology and providing potential therapeutic targets in precision medicine.

LncRNA SNHG16 Promotes the Proliferation and Metastasis of Oesophageal Squamous Cell Carcinoma by Interacting with EIF4A3 and Modulating Rhou mRNA Stability

LncRNA SNHG16 Promotes the Proliferation and Metastasis of Oesophageal Squamous Cell Carcinoma by Interacting with EIF4A3 and Modulating Rhou mRNA Stability

Abnormal Expression of SNHG7 Is a Biomarker for the Diagnosis and Prognosis of Neonatal Sepsis

Long non-coding RNA (lncRNA) is of great significance in diagnosing and prognosis of human diseases. This study aims to explore the expression of lncRNA SNHG7 in infants with neonatal sepsis and further evaluate the diagnostic and prognostic value of SNHG7 in neonatal sepsis. The expression levels of serum SNHG7 in 81 neonates were detected by quantitative real-time-PCR (qRT-PCR). The correlations between SNHG7 and clinicopathological indicators were estimated by the Pearson correlation coefficient. The receiver operating characteristic (ROC) curve was generated to assess the diagnostic value of SNHG7. Kaplan-Meier survival curve and multivariate Cox regression analysis were conducted to evaluate the prognostic value of SNHG7 in neonatal sepsis. The expression level of serum SNHG7 was significantly upregulated in the neonatal sepsis group compared to the controls, and overexpressed SNHG7 showed clinical diagnostic value for neonatal sepsis. It was observed that the SNHG7 levels were positively correlated with some indicators representing the degree of inflammation. Follow-up analysis and multivariate Cox regression revealed that the death probability of neonates with high SNHG7 level was higher than that with low SNHG7 levels, and SNHG7 was an independent factor of poor prognosis in neonates with neonatal sepsis. Together, our findings show that highly expressed SNHG7 has the potential to be a diagnostic biomarker for neonates with neonatal sepsis and was closely related to the poor prognosis of neonatal sepsis.

Characterization of inflammatory profiles and endothelial dysfunction in diabetic limb arterial occlusion.

Our study aims to detect the changes of adiponectin (APN), endothelin 1 (ET)-1, nitric oxide (NO), cystatin C (cysC) in diabetic limb arterial occlusion (DLAO) patients and unravel their associations with endothelial function. Total 240 type 2 diabetes mellitus (T2DM) patients were divided into a DM group (n = 80, ankle brachial index (ABI) ≥ 0.9) and a DLAO group (n = 160, ABI < 0.9). ABI, flow-mediated dilation (FMD) and nitroglycerin-mediated dilation (NMD), serum APN, ET-1, NO, and cysC were compared. There were significant increases in cysC and ET-1, and significant decreases in APN, NO, FMD and NMD of DLAO patients compared to T2DM patients. Serum APN and NO were positively correlated with ABI, while serum cysC and ET-1 were negatively correlated with ABI. cysC, ET-1 and diastolic blood pressure (DBP) were independent predictors of the severity of DLAO. Serum APN was positively correlated with FMD, NMD and NO, but was negatively correlated with ET-1 and cysC. FMD and NMD were positively correlated with APN and NO, and negatively correlated with ET-1 and cysC. Our study deciphers opposite roles of APN, NO, cysC and ET-1 in the development of DLAO and maintaining endothelial function.

LncRNA SNHG6 Silencing Could Arrest Progression of High Grade Colorectal Cancers.

Background & Objective:Colorectal cancer (CRC), like other cancers, needs faster and more accurate identifications. A well-timed prognosis of CRC could be an important turning point in the survival of patients. Supplementary signs, such as long non-coding RNAs (lncRNAs), could be helpful for this purpose. A new possible biomarker for CRC identification is introduced by this study. Methods: RNA extraction was performed by the RNX-Plus solution for 64 tumor and non-tumor tissues. Complementary DNAs (cDNAs) were synthesized, and quantitative real-time PCR was performed for relative expression level measurement and the data was analyzed statistically using the Prism 6 software. For Small nucleolar host gene 6 knockdown, siRNA was designed based on Reynolds rules. The cells were cultured in their appropriate media, and the siRNA-lipofectamine complex was formed. The transfection complex was presented for sw48, sw480, and sw1116 as CRC cells with different grades. After transfection, the SNHG6/β actin ratio was determined. Then, the distribution of siRNA-treated cells was determined by the Partec flow cytometer instrument and analyzed by the FloMax software.Results:SNHG6 was more expressed in CRC tumors than non-tumor tissues. In tumor tissues, SNHG6 upregulation and tumors’ grade progression were concurrent. SNHG6 was upregulated in cases with lymphovascular invasion than in cases with perineural invasion. The knockdown of SNHG6 conduced to G1 arrest in CRC cells, more noticeably in high-grade ones. Conclusion:SNHG6 could be applied as a consideration to differentiate tumor and non-tumor tissues and grade definition in colorectal malignancies, and it could participate in colorectal tumor formation as a cell cycle progressive factor.

Long noncoding RNA small nucleolar RNA host gene 12/microRNA-138-5p/nuclear factor I/B regulates neuronal apoptosis, inflammatory response, and oxidative stress in Parkinson’s disease

ABSTRACT Parkinson’s disease (PD) is a progressive neurodegenerative disorder that causes tremors, gait rigidity, and hypokinesia. We determined the effects of long noncoding RNA small nucleolar RNA host gene 12 (lncRNA SNHG12) on the development of PD. StarBase analysis and dual-luciferase reporter assay verified the interaction between lncRNA SNHG12 and microRNA-138-5p (miR-138-5p). The effects of suppressed lncRNA SNHG12 and increased miR-138-5p levels on mRNA were determined using quantitative real-time-PCR (qRT-PCR) in 1-methyl-4-phenylpyridinium (MPP+) treated SH-SY5Y cells. Increased lactate dehydrogenase (LDH) activity, apoptosis, cleaved-Caspase3/Caspase3 ratio, inflammatory response, reactive oxygen species (ROS) level, decreased cell viability, and superoxide dismutase (SOD) activity were observed in MPP+-stimulated SH-SY5Y cells. Transfection of the lncRNA SNHG12-plasmid reduced neuronal apoptosis, inflammation, and oxidative stress in MPP+-stimulated SH-SY5Y cells that were rescued by adding the miR-138-5p mimic. These results showed that lncRNA SNHG12 could affect neuronal apoptosis, inflammation, and oxidative stress in a PD cell model by regulating miR-138-5p expression. TargetScan and dual-luciferase reporter analysis suggested that miR-138-5p targeted nuclear factor I/B (NFIB). Furthermore, the expression level of NFIB was downregulated after MPP+ stimulation in SH-SY5Y cells. After transfecting with the miR-138-5p inhibitor, NFIB-siRNA, and co-transfecting and detecting NFIB mRNA and protein, we found that miR-138-5p negatively regulated NFIB expression. In conclusion, lncRNA SNHG12 could alleviate neuronal apoptosis, inflammation, and oxidative stress in a PD cell model by regulating the miR-138-5p/NFIB axis, providing new therapeutic targets for patients with PD.

LncRNA SNHG3 promotes gastric cancer cell proliferation and metastasis by regulating the miR-139-5p/MYB axis.

The long non-coding RNA (lncRNA) SNHG3 has been shown to play oncogenic roles in several cancer types, but the mechanisms underlying its activity are poorly understood. In this study, we aimed to explore the clinical relevance and mechanistic role of SNHG3 in gastric cancer (GC). We found that SNHG3 expression in GC cell lines and tissues was significantly increased, and the upregulation of this lncRNA was correlated with tumor clinical stage and decreased patient survival. Knocking down SNHG3 in GC cells impaired the proliferative, migratory, and invasive activity in vitro and constrained in vivo GC xenograft tumor growth. Mechanistically, SNHG3 was found to bind and sequester miR-139-5p, thereby indirectly promoting the upregulation of the miR-139-5p target gene MYB. These data demonstrated that SNHG3 functions in an oncogenic manner to drive GC proliferation, migration, and invasion by regulating the miR-139-5p/MYB axis.

Regulatory mechanism of the SNHG3/miR-302a-3p/E2F1 feedback loop in nerve repair post cerebral ischemic stroke

Cerebral ischemic stroke (CIS) remains a primary cause of death worldwide. The current knowledge has identified the implication of microRNAs (miRNAs) in the pathophysiology of CIS. This study investigated the mechanism of miR-302a-3p in nerve repair post CIS. A middle cerebral artery occlusion (MCAO) model was established in mice to simulate CIS. miR-302a-3p expression in brain tissues of MCAO mice was up-regulated by injecting agomiR-302a-3p. Neurological deficits of MCAO mice were evaluated through neurological function score, forelimb placing test, and balance beam walking test. Neuronal damage was measured using Nissl staining. The concentrations of nerve injury-related factors (S100B and GFAP) and the contents of neuroinflammatory factors (TNF-α and IL-1β) in serum were examined using ELISA kits. miR-302a-3p, E2F1, and long non-coding RNA (lncRNA) SNHG3 expressions in brain tissues of MCAO mice were determined using RT-qPCR and Western blot. The binding relationships between miR-302a-3p and E2F1 and E2F1 and SNHG3 were validated using dual-luciferase and ChIP assays, respectively. miR-302a-3p expression was reduced in brain tissues of MCAO mice. miR-302a-3p overexpression increased the number of neurons, decreased the concentrations of S100B and GFAP, reduced the contents of TNF-α and IL-1β, promoted nerve repair, and alleviated CIS-induced brain injury. miR-302a-3p targeted E2F1 expression, and E2F1 activated SNHG3 transcription. E2F1 overexpression or SNHG3 overexpression reversed the effect of miR-302a-3p overexpression on nerve repair in MCAO mice. miR-302a-3p overexpression repressed SNHG3 transcription by targeting E2F1 expression, thereby promoting nerve repair and alleviating CIS.