Small Nucleolar RNA Host Gene 1 Overexpression Research Articles

Long non‑coding RNA SNHG1 promotes autophagy in vascular smooth muscle cells induced by facilitating CLEC7A.

Long non‑coding RNAs serve a crucial role in autophagy of vascular smooth muscle cells (VSMCs). The present study aimed to investigate the effect of small nucleolar RNA host gene 1 (SNHG1) on autophagy in VSMCs and the associated underlying mechanisms. Rapamycin was used to induce autophagy in VSMCs and the effects of SNHG1 on the proliferation and migration of VSMCs and the change in phenotype were tested following overexpression and silencing of SNHG1. The target gene of SNHG1 was predicted and validated. SNHG1‑regulated autophagy of VSMCs via C‑type lectin domain family 7 member A (CLEC7A) was determined by combined silencing of SNHG1 and overexpression of CLEC7A. Rapamycin‑induced autophagy in VSMCs changed the cell phenotype from contractile to synthetic, with decreased expression of α‑smooth muscle actin and smooth muscle protein 22a and increased expression of osteopontin. Overexpression of SNHG1 caused the same change in phenotype while the opposite change was observed following SNHG1 silencing. Overexpression of SNHG1 promoted the proliferation and migration of VSMCs. CLEC7A was identified as a target gene of SNHG1 and a direct binding relationship between them was confirmed by RNA immunoprecipitation and RNA pull‑down assays. Overexpression of SNHG1 increased the expression of CLEC7A. The expression of both SNHG1 and CLEC7A was increased during autophagy of VSMCs. Overexpression of SNHG1 promoted autophagy of VSMCs and silencing of CLEC7A reduced this effect of SNHG1. In conclusion, SNHG1 and CLEC7A were increased in VSMCs following autophagy. SNHG1 promotes the conversion of VSMCs from a contractile phenotype to a synthetic phenotype by facilitating CLEC7A expression.

Abstract 1552: Tumorigenesis of basal muscle invasive bladder cancer was mediated by PTEN protein degradation resulting from SNHG1 upregulation

Abstract hosphatase and tensin homolog deleted on chromosome ten (PTEN) serves as a powerful tumor suppressor, and has been found to be downregulated in human bladder cancer (BC) tissues. Despite this observation, the mechanisms contributing to PTEN’s downregulation have remained elusive. In this study, we discovered that mice exposed to N-butyl-N-(4-hydroxybu-tyl)nitrosamine (BBN), a specific bladder chemical carcinogen, exhibited primary basal muscle invasive BC (BMIBC) accompanied by a pronounced reduction in PTEN protein expression in vivo. Utilizing a lncRNA deep sequencing high-throughput platform, along with gain- and loss-of-function analyses, we identified small nucleolar RNA host gene 1 (SNHG1) as a critical lncRNA that might drive the formation of primary BMIBCs in BBN-treated mice. Cell culture results further demonstrated that BBN exposure significantly induced SNHG1 in normal human bladder urothelial cell UROtsa. Notably, the ectopic expression of SNHG1 alone was sufficient to induce malignant transformation in human urothelial cells, while SNHG1 knockdown effectively inhibited anchorage-independent growth of human BMIBCs. Our detailed investigation revealed that SNHG1 overexpression led to PTEN protein degradation through its direct interaction with HUR. This interaction reduced HUR binding to ubiquitin-specific peptidase 8 (USP8) mRNA, causing degradation of USP8 mRNA and a subsequent decrease in USP8 protein expression. The downregulation of USP8, in turn, increased PTEN poly-ubiquitination and degradation, culminating in cell malignant transformation and BMIBC anchorage-independent growth. In vivo studies confirmed the downregulation of PTEN and USP8, as well as their positive correlations in both BBN-treated mouse bladder urothelium and tumor tissues of bladder cancer in nude mice.Our findings, for the first time, demonstrate that overexpressed SNHG1 competes with USP8 for binding to HUR. This competition attenuates USP8 mRNA stability and protein expression, leading to PTEN protein degradation, consequently, this process drives urothelial cell malignant transformation and fosters BMIBC growth and primary BMIBC formation. Citation Format: Chuanshu Huang, Tengda Li, Honglei Jin. Tumorigenesis of basal muscle invasive bladder cancer was mediated by PTEN protein degradation resulting from SNHG1 upregulation [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 1552.

Tumorigenesis of basal muscle invasive bladder cancer was mediated by PTEN protein degradation resulting from SNHG1 upregulation

BackgroundPhosphatase and tensin homolog deleted on chromosome ten (PTEN) serves as a powerful tumor suppressor, and has been found to be downregulated in human bladder cancer (BC) tissues. Despite this observation, the mechanisms contributing to PTEN’s downregulation have remained elusive.MethodsWe established targeted genes’ knockdown or overexpressed cell lines to explore the mechanism how it drove the malignant transformation of urothelial cells or promoted anchorageindependent growth of human basal muscle invasive BC (BMIBC) cells. The mice model was used to validate the conclusion in vivo. The important findings were also extended to human studies.ResultsIn this study, we discovered that mice exposed to N-butyl-N-(4-hydroxybu-tyl)nitrosamine (BBN), a specific bladder chemical carcinogen, exhibited primary BMIBC accompanied by a pronounced reduction in PTEN protein expression in vivo. Utilizing a lncRNA deep sequencing high-throughput platform, along with gain- and loss-of-function analyses, we identified small nucleolar RNA host gene 1 (SNHG1) as a critical lncRNA that might drive the formation of primary BMIBCs in BBN-treated mice. Cell culture results further demonstrated that BBN exposure significantly induced SNHG1 in normal human bladder urothelial cell UROtsa. Notably, the ectopic expression of SNHG1 alone was sufficient to induce malignant transformation in human urothelial cells, while SNHG1 knockdown effectively inhibited anchorage-independent growth of human BMIBCs. Our detailed investigation revealed that SNHG1 overexpression led to PTEN protein degradation through its direct interaction with HUR. This interaction reduced HUR binding to ubiquitin-specific peptidase 8 (USP8) mRNA, causing degradation of USP8 mRNA and a subsequent decrease in USP8 protein expression. The downregulation of USP8, in turn, increased PTEN polyubiquitination and degradation, culminating in cell malignant transformation and BMIBC anchorageindependent growth. In vivo studies confirmed the downregulation of PTEN and USP8, as well as their positive correlations in both BBN-treated mouse bladder urothelium and tumor tissues of bladder cancer in nude mice.ConclusionsOur findings, for the first time, demonstrate that overexpressed SNHG1 competes with USP8 for binding to HUR. This competition attenuates USP8 mRNA stability and protein expression, leading to PTEN protein degradation, consequently, this process drives urothelial cell malignant transformation and fosters BMIBC growth and primary BMIBC formation.

LncRNA SNHG1 promotes nasopharyngeal carcinoma development via targeting miR-424-5p.

Nasopharyngeal carcinoma (NPC) is a malignant tumor of the head and neck. Distant metastasis and drug resistance are the main causes of cancer-related death. A better understanding of the molecular mechanisms that affect the progression of NPC would contribute to clinical treatment. This paper aims to investigate the effects of the long noncoding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) on biological phenotypes of NPC cells and its related mechanisms. The expression of SNHG1 and miR-424-5p in non-cancerous nasopharyngeal mucosa tissues and NPC tissues, as well as in normal nasopharyngeal epithelial cells and NPC cells was detected by qRT-PCR. HK1 and C666-1 cells were transfected with SNHG1 overexpression vector (OE-SNHG1), miR-424-5p mimic, SNHG1 knockdown vector (sh-SNHG1), or miR-424-5p inhibitor, followed by detection of transfection efficiency by qRT-PCR, cell viability by MTT, and invasive and migratory abilities by transwell invasion assay and cell scratch test. Moreover, the relationship between SNHG1 and miR-424-5p was detected by dual-luciferase reporter and RIP assays. In NPC tissues and cells, SNHG1 was upregulated but miR-424-5p was downregulated. Transfection with OE-SNHG1 or miR-424-5p inhibitor promoted proliferative, invasive, and migratory phenotypes of HK1 and C666-1 cells; transfection of sh-SNHG1 or mi-miR-424-5p induced reverse trends. Mechanistically, SNHG1 negatively regulated miR-424-5p expression, and transfection of miR-424-5p inhibitor counteracted the inhibitory effects of sh-SNHG1 on the proliferative, invasive, and migratory phenotypes of HK1 and C666-1 cells. LncRNA SNHG1 promoted proliferation, invasion and migration of NPC cells by repressing miR-424-5p expression.

Role and mechanism of the lncRNA SNHG1/miR‑450b‑5p/IGF1 axis in the regulation of myocardial ischemia reperfusion injury.

The increasing rates of morbidity and mortality caused by ischemic heart disease pose a serious threat to human health. Long non-coding (lnc)RNA small nucleolar RNA host gene 1 (SNHG1) has a protective effect on the myocardium. In the present study, the role of lncRNA SNHG1 in myocardial ischemia reperfusion injury (MIRI) and the underlying mechanisms were investigated. After hypoxia/reoxygenation (H/R) induction, the expression levels of lncRNA SNHG1 were detected using reverse transcription-quantitative PCR. After lncRNA SNHG1 overexpression via cell transfection, cell viability was detected using an MTT assay, apoptotic rates were detected using TUNEL staining, apoptosis-related protein expression levels were detected using western blotting and respective kits were used to measure the oxidative stress levels. The Encyclopedia of RNA Interactomes database predicted the presence of binding sites between lncRNA SNHG1 and microRNA (miR)-450b-5p, and between miR-450b-5p and insulin-like growth factor 1 (IGF1). These interactions were then verified using luciferase reporter assays. Subsequently, the regulatory mechanism underlying the lncRNA SNHG1/miR-450b-5p/IGF1 axis in MIRI was investigated by overexpressing miR-450b-5p and knocking down IGF1 expression in H/R-induced cells. Finally, the expression of PI3K/Akt signaling pathway-related proteins was detected using western blotting. lncRNA SNHG1 expression was significantly downregulated in H/R-induced AC16 cells. lncRNA SNHG1 overexpression significantly inhibited apoptosis and decreased oxidative stress levels in H/R-induced AC16 cells, which was mediated via regulation of the miR-450b-5p/IGF1 axis and activation of the PI3K/Akt signaling pathway. Therefore, the present study suggested that activation of the PI3K/Akt signaling pathway via the lncRNA SNHG1/miR-450b-5p/IGF1 axis inhibited the apoptosis and oxidative stress levels of H/R-induced AC16 cells.

Positive feedback loop of lncRNA SNHG1/miR‑16‑5p/GATA4 in the regulation of hypoxia/reoxygenation‑induced cardiomyocyte injury.

Numerous studies have demonstrated that long non-coding RNAs (lncRNAs) serve an important regulatory role in ischemic injury of cardiomyocytes. lncRNA small nucleolar RNA host gene 1 (SNHG1) could effectively protect cardiomyocytes against various injuries. However, the role of SNHG1 in ischemic cardiomyocyte injury is unclear. It was hypothesized that SNHG1 may have a protective effect on cardiomyocyte injury induced by hypoxia/reoxygenation (H/R) by sponging microRNA (miRNA/miR). The purpose of the present study was to explore the role and molecular mechanism of SNHG1 in ischemic cardiomyocyte injury. A H9c2 cardiomyocyte H/R model was established. The expression levels of SNHG1 in cardiomyocytes treated with H/R were detected using reverse transcription-quantitative PCR. A luciferase reporter assay was used to analyze the associations among SNHG1, miR-16-5p and GATA binding protein 4 (GATA4). Chromatin immunoprecipitation experiments were performed to analyze the interaction between SNHG1 and GATA4. Cell Counting Kit-8, enzyme-linked immunosorbent assay, terminal deoxynucleotidyl-transferase-mediated dUTP nick end labeling and western blotting experiments were used to detect cell activity, lactate dehydrogenase release, apoptosis and apoptosis-related proteins (Bcl-2, Bax, Cleaved caspase-3 and Cleaved caspase-9), respectively. The expression levels of SNHG1 were downregulated in cardiomyocytes treated with H/R. Overexpression of SNHG1 had a protective effect on cardiomyocyte injury induced by H/R. In addition, SNHG1 could regulate the expression levels of GATA4 via sponging of miR-16-5p. Further experiments revealed that GATA4 could bind to the promoter region of SNHG1 and subsequently regulated the expression levels of SNHG1, indicating the important role of the positive feedback loop of SNHG1/miR-16-5p/GATA4 in cardiomyocyte ischemic injury. To conclude, the present study revealed the protective effect of the SNHG1/miR-16-5p/GATA4 positive feedback loop on cardiomyocyte injury induced by H/R and provided a potential therapeutic target for ischemic cardiomyocyte injury.

Long non-coding RNA SNHG1 relieves microglia activation by downregulating miR-329-3p expression in an in vitro model of cerebral infarction.

Following cerebral infarction, activated microglia cells can release a large amount of inflammatory cytokines, thereby exacerbating neuronal damage. It has been demonstrated that the long non-coding RNA small nucleolar RNA host gene 1 (SNHG1) exerts a protective effect against cerebral infarction. However, its specific role in cerebral infarction and underlying mechanism have yet to be fully elucidated. The present study aimed to investigate the effects of the SNHG1 and microRNA (miR)-329-3p in cerebral infarction and to determine the underlying molecular mechanisms. An in vitro oxygen-glucose deprivation (OGD) model was established using the BV-2 microglial cell line. The mRNA expression levels of SNHG1 and miR-329-3p were analyzed using reverse transcription-quantitative PCR and the protein expression levels of cleaved caspase-3 and caspase-3 were detected using western blotting. The binding relationship between SNHG1 and miR-329-3p was predicted using starBase and verified using a dual luciferase reporter assay. The release of TNF-α and nitric oxide, as well as caspase-3 activity, were detected using appropriate commercial kits. Flow cytometry analysis was performed to measure cell apoptosis. The results of the present study revealed that the expression levels of SNHG1 were upregulated in the OGD-induced BV-2 cell model. miR-329-3p was discovered to directly target SNHG1, and its mRNA expression levels were downregulated in the OGD-induced BV-2 cell model. The SNHG1-plasmid downregulated miR-329-3p expression levels, while this effect was reversed by transfection with the miR-329-3p mimic. The overexpression of SNHG1 or knockdown of miR-329-3p inhibited OGD-induced BV-2 cell activation. In conclusion, the results of the present study suggested that SNHG1 may reduce microglial cell activity by regulating the expression of miR-329-3p, indicating its potential protective role in cerebral infarction.

Long non-coding RNA small nucleolar RNA host gene 1 alleviates the progression of epilepsy by regulating the miR-181a/BCL-2 axis in vitro

PurposeLong non-coding RNAs (lncRNAs) have been reported to be involved in regulating epilepsy. The purpose of this study is to investigate the possibly regulatory mechanism of small nucleolar RNA host gene 1 (SNHG1) on epilepsy. MethodsQuantitative real-time PCR was utilized to detect the expression of SNHG1, microRNA (miR)-181a, and B-cell lymphoma-2 (BCL-2). Through an enzyme-linked immunosorbent assay, the levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, and cyclooxygenase-2 (COX-2) were determined. The viability and apoptosis of CTX-TNA2 cells were measured using MTT assay and flow cytometry analysis, respectively. Western blot assay was performed to analyze the protein levels of Bcl-2, BCL2-associated X, and Caspase-3. The relationships between miR-181a and SNHG1/BCL-2 were confirmed by the dual-luciferase reporter assay. ResultsSNHG1 expression was down-regulated in EP tissues and kainic acid (KA)-induced CTX-TNA2 cells. The apoptosis and release of inflammatory factors (TNF-α, IL-1β, IL-6, and COX-2) in KA-induced CTX-TNA2 cells were suppressed by SNHG1 overexpression and promoted by miR-181a up-regulation. In addition, we confirmed that SNHG1 targeted miR-181a, whereas BCL-2 was a target gene of miR-181a. Negative correlations between SNHG1 and miR-181a, as well as miR-181a and BCL-2 were exhibited. Both the up-regulation of miR-181a and down-regulation of BCL-2 reversed the inhibiting effects of SNHG1 on apoptosis and inflammatory response of KA-induced CTX-TNA2 cells, and the promoting effect upon cell viability. ConclusionsSNHG1 alleviated the progression of EP by modulating the miR-181a/BCL-2 axis in vitro, thus SNHG1 could act as a possible therapeutic target for treating EP.

SNHG1 promotes proliferation, migration and invasion of bladder cancer cells via the PI3K/AKT signaling pathway.

Long non-coding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) has been previously reported to mediate a number of functions during the progression of cancer. However, its involvement in bladder cancer remain unclear. The aim of the present study was to investigate the expression of SNHG1 in bladder cancer and to identify its potential mechanisms. SNHG1 expression was firstly detected in cancer tissues and cells. The effects of SNHG1 on the malignant phenotypes were then investigated. Furthermore, the influence of SNHG1 on the PI3K/AKT signaling pathway was examined. It was demonstrated that SNHG1 expression was significantly upregulated in bladder cancer tissues and cells. Moreover, the loss-of-function experimental results suggested that knockdown of SNHG1 inhibited bladder cancer cell proliferation, migration and invasion, but increased apoptosis; however, SNHG1 overexpression promoted these processes. Mechanistically, rescue assays identified that SNHG1 activated the PI3K/AKT signaling pathway. Therefore, it was speculated that SNHG1 functioned as a carcinogenic lncRNA in bladder cancer via activation of PI3K/AKT.

LncRNA SNHG1 attenuates osteogenic differentiation via the miR‑101/DKK1 axis in bone marrow mesenchymal stem cells.

The imbalance induced by inhibition of bone mesenchymal stem cell (BMSC) osteogenic differentiation results in osteoporosis (OP); however, the underlying regulatory mechanism is not completely understood. Long non-coding RNAs (lncRNAs) serve crucial roles in osteogenic differentiation; therefore, investigating their regulatory role in the process of osteogenic differentiation may identify a promising therapeutic target for OP. The expression of small nucleolar RNA host gene 1 (SNHG1), Dickkopf 1 (DKK1), microRNA (miR)-101, RUNX family transcription factor 2 (RUNX2), osteopontin (OPN) and osteocalin (OCN) were detected via reverse transcription-quantitative PCR. The protein expression levels of DKK1, β-catenin, RUNX2, OPN, OCN, osterix and collagen type I α1 chain were analyzed by performing western blotting. The osteoblastic phenotype was assessed by conducting alkaline phosphatase activity detection and Alizarin Red staining. The interaction between SNHG1 and miR-101 was validated by bioinformatics and luciferase assays. The regulatory role of SNHG1 in BMSC osteogenic differentiation was assessed. SNHG1 expression was downregulated in a time-dependent manner during the process of osteogenic differentiation. SNHG1 overexpression inhibited osteogenic differentiation compared with the pcDNA group. The results indicated that SNHG1 and DKK1 directly interacted with miR-101. Moreover, SNHG1 regulated the Wnt/β-catenin signaling pathway to inhibit osteogenic differentiation via the miR-101/DKK1 axis. The present study indicated that lncRNA SNHG1 could attenuate BMSC osteogenic differentiation via the miR-101/DKK1 axis as a competitive endogenous RNA. Therefore, the present study furthered the current understanding of the potential mechanism underlying lncRNAs in in osteogenic differentiation.

LncRNA SNHG1 Knockdown Alleviates Amyloid-β-Induced Neuronal Injury by Regulating ZNF217 via Sponging miR-361-3p in Alzheimer's Disease.

Long noncoding RNAs have been proven to play an important role in the progression of Alzheimer's disease (AD). However, the function of small nucleolar RNA host gene 1 (SNHG1) in AD progression remains to be studied. To explore the role of SNHG1 in AD progression and clarify its potential mechanism. Amyloid β-protein (Aβ) was used to construct an AD cell model in vitro. The expression levels of SNHG1 and miR-361-3p were determined by quantitative real-time polymerase chain reaction. Cell viability and apoptosis were measured by cell counting kit 8 assay and flow cytometry. The levels of apoptosis-related proteins and zinc finger gene 217 (ZNF217) protein were evaluated by western blot analysis. Additionally, the contents of inflammatory cytokines and oxidative stress markers were tested by enzyme-linked immunosorbent assay. Furthermore, dual-luciferase reporter and RNA immunoprecipitation assays were used to verify the interaction between miR-361-3p and SNHG1 or ZNF217. Aβ could induce cell injury, while resveratrol could reverse this effect. SNHG1 expression was positively regulated by Aβ and negatively regulated by resveratrol. SNHG1 knockdown could reverse the promotion effect of Aβ on cell injury. Moreover, SNHG1 sponged miR-361-3p, and miR-361-3p targeted ZNF217. Additionally, miR-361-3p overexpression reversed the promotion effect of SNHG1 overexpression on cell injury, and ZNF217 silencing also reversed the promotion effect of miR-361-3p inhibitor on cell injury. SNHG1 promoted cell injury by regulating the miR-361-3p/ZNF217 axis, which might provide a theoretical basis for molecular therapy of AD.

LncRNA SNHG1 contributes to the regulation of acute myeloid leukemia cell growth by modulating miR-489-3p/SOX12/Wnt/β-catenin signaling.

The long noncoding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) is a critical regulator for the development and progression of multiple tumors. Yet, the role of SNHG1 in acute myeloid leukemia (AML) is unknown. The present study demonstrated that SNHG1 expression was upregulated in AML. SNHG1 silencing markedly repressed AML cell growth, whereas SNHG1 overexpression had the opposite effect. MicroRNA-489-3p (miR-489-3p) was identified as a SNHG1-targeting miRNA. SNHG1 knockdown increased miR-489-3p expression. Low expression of miR-489-3p was correlated with high expression of SNHG1 in AML tissues. miR-489-3p overexpression restricted AML cell growth, and SRY-related high-mobility-group box 12 (SOX12) was identified as a miR-489-3p-targeting gene. SNHG1 inhibition or miR-489-3p overexpression inactivated Wnt/β-catenin signaling through downregulation of SOX12. SOX12 overexpression partially reversed the SNHG1 knockdown- or miR-489-3p overexpression-mediated effects. Taken together, these data indicate that suppression of SNHG1 downregulates AML cell growth by inactivating SOX12/Wnt/β-catenin signaling via upregulating miR-489-3p.

LncRNA SNHG1 exerts a protective role in cardiomyocytes hypertrophy via targeting miR-15a-5p/HMGA1 axis.

Heart failure preceded by pathological cardiac hypertrophy is a leading cause of death. Long noncoding RNA small nucleolar RNA host gene 1 (SNHG1) was reported to inhibit cardiomyocytes apoptosis, but the role and underlying mechanism of SNHG1 in pathological cardiac hypertrophy have not yet been understood. This study was designed to investigate the role and molecular mechanism of SNHG1 in regulating cardiac hypertrophy. We found that SNHG1 was upregulated during cardiac hypertrophy both in vivo (transverse aortic constriction treatment) and in vitro (phenylephrine [PE] treatment). SNHG1 overexpression attenuated the cardiomyocytes hypertrophy induced by PE, while SNHG1 inhibition promoted hypertrophic response of cardiomyocytes. Furthermore, SNHG1 and high-mobility group AT-hook 1 (HMGA1) were confirmed to be targets of miR-15a-5p. SNHG1 promoted HMGA1 expression by sponging miR-15a-5p, eventually attenuating cardiomyocytes hypertrophy. There data revealed a novel protective mechanism of SNHG1 in cardiomyocytes hypertrophy. Thus, targeting of SNHG1-related pathway may be therapeutically harnessed to treat cardiac hypertrophy.

High expression of lncRNA SNHG1 in prostate cancer patients and inhibition of SNHG1 suppresses cell proliferation and promotes apoptosis.

This study aimed to investigate the expression of long non-coding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) in prostate cancer (PCa) patients and to assess the effects of SNHG1 on PCa cell proliferation and apoptosis. A total of 134 PCa patients were randomly included from patients who underwent surgical resection at our hospital from October 2015 to December 2016. The SNHG1 expression levels in PCa tissues and paired adjacent non-cancerous tissues were detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR). The association of the SNHG1 expression with clinical-pathological features of PCa patients was summarized and evaluated. A short interfering (si) RNA targeting SNHG1 and pcDNA3.1-SNHG1 were transfected into PC3 and DU145 PCa cell lines, and transfection efficiency was verified by qRT-PCR. Cell proliferation and apoptosis were assessed by methylthiazolyldiphenyl-tetrazolium bromide (MTT) and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assays, respectively. The SNHG1 expression was significantly upregulated in PCa tumor tissues compared with paired adjacent non-cancerous tissues. The SNHG1 expression was obviously associated with the TNM stage, Gleason Score, lymph node invasion, and long-term metastasis mortality rate. Silencing of SNHG1 inhibited cell proliferation and promoted apoptosis in PC3 and DU145 PCa cell lines in vitro, while overexpression of SNHG1 led to opposite results. LncRNA SNHG1 was upregulated and associated with aggressive malignant behavior in PCa progression. SNHG1 might serve as a potential prognostic biomarker and potential therapeutic target for PCa.

Long non-coding RNA SNHG1 protects human AC16 cardiomyocytes from doxorubicin toxicity by regulating miR-195/Bcl-2 axis.

Doxorubicin (DOX) is a highly effective anti-tumor drug, but its cardiotoxicity largely restricts its clinical application. The present study was designed to explore whether in vitro DOX toxicity in AC16 cardiomyocytes can be regulated by long non-coding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) and to elucidate the underlying mechanisms. We found that DOX treatment led to severe damage in AC16 cells through decreasing cell viability and increasing cell apoptosis. DOX treatment also reduced the expression of SNHG1 in AC16 cells, and overexpression of SNHG1 alleviated the increased apoptosis in DOX-treated AC16 cells. Moreover, we found that SNHG1 could counteract the inhibitory effect of miR-195 on Bcl-2, and miR-195 restoration blocked the beneficial effect of SNHG1 against DOX toxicity in AC16 cells. In short, the present study provided convincing evidence that SNHG1 protects human AC16 cardiomyocytes from DOX toxicity partly by regulating miR-195/Bcl-2 axis.

The Interaction Between lncRNA SNHG1 and miR-140 in Regulating Growth and Tumorigenesis via the TLR4/NF-κB Pathway in Cholangiocarcinoma.

Cholangiocarcinoma (CCA) is the second most common primary hepatobiliary carcinoma. The long noncoding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) has been reported to contribute to the progression of multiple cancers. Nonetheless, the functions and hidden mechanism of SNHG1 remain unclear in CCA. In this study, the SNHG1 levels were boosted in CCA cell lines, and knockdown of SNHG1 repressed CCA cell proliferation and invasion in vitro. The data also demonstrated that miR-140 could act as a target of SNHG1 in CCA and inhibited CCA cell proliferation and invasion, whereas the inhibition effects were relieved by overexpression of SNHG1. In addition, Toll-like receptor 4 (TLR4), an NF-κB-activating signal, was identified to be a target of miR-140. SNHG1, as a competing endogenous RNA (ceRNA) for miR-140, enhanced TLR4 expression and activated NF-κB signaling, thereby regulating growth and tumorigenesis in CCA. Animal experiments further confirmed this conclusion. Collectively, these findings not only uncovered a key role of SNHG1/miR-140/TLR4/NF-κB signaling axis in CCA tumorigenesis and progression but also denoted the probable utilization of SNHG1 as a therapeutic target for CCA.

LncRNA SNHG1 correlates with higher T stage and worse overall survival, and promotes cell proliferation while reduces cell apoptosis in breast cancer.

BackgroundThe aim of this study was to investigate the correlation of long non-coding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) with the prognosis in breast cancer patients, and its effect on breast cancer cell proliferation and apoptosis.MethodsA total of 178 breast cancer patients were consecutively recruited, then tumor tissue and the paired adjacent tissue were obtained during surgery for lncRNA SNHG1 determination by quantitative polymerase chain reaction (qPCR). LncRNA SNHG1 expression was also measured in breast cancer cell lines and normal breast epithelial cell line. Subsequently, negative control (NC) overexpression plasmids, lncRNA SNHG1 overexpression plasmids, NC short hairpin RNA (shRNA) plasmids and lncRNA SNHG1 shRNA plasmids were transfected into MDA-MB-453 cells as well as MCF7 cells, and cell proliferation and apoptosis were measured afterward.ResultsLncRNA SNHG1 expression in tumor tissue was increased compared with paired adjacent tissue, and it correlated with higher T stage and worse overall survival (OS) in breast cancer patients. LncRNA SNHG1 expression was also elevated in breast cancer cell lines compared with normal breast epithelial cell line. Cell Counting Kit-8 (CCK8) assay revealed that lncRNA SNHG1 overexpression promoted while lncRNA SNHG1 shRNA reduced cell proliferation, and Annexin V-fluorescein isothiocyanate/propidium iodide staining (AV/PI) assay illustrated that lncRNA SNHG1 overexpression decreased while lncRNA SNHG1 shRNA increased cell apoptosis rate. In addition, Western Blot assay disclosed that lncRNA SNHG1 overexpression downregulated while lncRNA SNHG1 shRNA upregulated pro-apoptotic marker (C-Caspase3) expression, and lncRNA SNHG1 overexpression increased while lncRNA SNHG1 shRNA decreased anti-apoptotic marker (p-P38) expression.ConclusionsLncRNA SNHG1 is upregulated in tumor tissue and correlates with higher T stage and worse OS, and it promotes cell proliferation but inhibits cell apoptosis in breast cancer.

LncRNA SNHG1 correlates with higher T stage and worse overall survival, and promotes cell proliferation while reduces cell apoptosis in breast cancer

Background: The aim of this study was to investigate the correlation of long non-coding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) with the prognosis in breast cancer patients, and its effect on breast cancer cell proliferation and apoptosis. Methods: A total of 178 breast cancer patients were consecutively recruited, then tumor tissue and the paired adjacent tissue were obtained during surgery for lncRNA SNHG1 determination by quantitative polymerase chain reaction (qPCR). LncRNA SNHG1 expression was also measured in breast cancer cell lines and normal breast epithelial cell line. Subsequently, negative control (NC) overexpression plasmids, lncRNA SNHG1 overexpression plasmids, NC short hairpin RNA (shRNA) plasmids and lncRNA SNHG1 shRNA plasmids were transfected into MDA-MB-453 cells as well as MCF7 cells, and cell proliferation and apoptosis were measured afterward. Results: LncRNA SNHG1 expression in tumor tissue was increased compared with paired adjacent tissue, and it correlated with higher T stage and worse overall survival (OS) in breast cancer patients. LncRNA SNHG1 expression was also elevated in breast cancer cell lines compared with normal breast epithelial cell line. Cell Counting Kit-8 (CCK8) assay revealed that lncRNA SNHG1 overexpression promoted while lncRNA SNHG1 shRNA reduced cell proliferation, and Annexin V-fluorescein isothiocyanate/propidium iodide staining (AV/PI) assay illustrated that lncRNA SNHG1 overexpression decreased while lncRNA SNHG1 shRNA increased cell apoptosis rate. In addition, Western Blot assay disclosed that lncRNA SNHG1 overexpression downregulated while lncRNA SNHG1 shRNA upregulated pro-apoptotic marker (C-Caspase3) expression, and lncRNA SNHG1 overexpression increased while lncRNA SNHG1 shRNA decreased anti-apoptotic marker (p-P38) expression. Conclusions: LncRNA SNHG1 is upregulated in tumor tissue and correlates with higher T stage and worse OS, and it promotes cell proliferation but inhibits cell apoptosis in breast cancer.

Long Noncoding RNA Small Nucleolar RNA Host Gene 1 (SNHG1) Promotes Renal Cell Carcinoma Progression and Metastasis by Negatively Regulating miR-137.

BackgroundData on the expression of RCC tissues from the GEO database and patient survival data from TCGA were used to explore the prognostic significance of long noncoding RNA SNHG1. SNHG1 has been reported to participate in the development of several cancers, but, the underlying mechanism of SNHG1 in renal cell carcinoma (RCC) has not been reported. The purpose of our study was to investigate the potential function of SNHG1 in RCC.Material/MethodsThe expression of SNHG1 in 40 cases of RCC and adjacent normal tissues and 5 cell lines was detected by qRT-PCR. Cell proliferation, Transwell assay, and Western blotting assay were carried out to investigate the biological function of SNHG1. A rescue experiment was performed to verify that miR-137 can partly impede the effect of SNHG1 on renal cancer cells.ResultsSNHG1 was identified to be overexpressed in RCC tissues and RCC cell lines. High levels of SNHG1 were correlated with poor prognosis of RCC patients. Knockdown of SNHG1 suppressed the proliferation, invasion, and EMT capacity in RCC. Moreover, miR-137 abrogated the effect of SNHG1 on RCC.ConclusionsSNHG1 is significantly upregulated in RCC and renal cancer cell lines. Overexpression of SNHG1 participates in RCC tumorigenesis by regulating miR-137.

Long non-coding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) promote cell proliferation in colorectal cancer by affecting P53.

Colorectal cancer (CRC) is one of the most frequent malignant tumors worldwide. The connection between lncRNAs expression and CRC development has not been well identified in the recent literature. This study focuses on the role of lncRNA-SNHG1 on CRC progression and development. The quantitative Real-time PCR (qRT-PCR) assay was conducted to identify the expression level of small nucleolar RNA host gene 1 (SNHG1). Cell proliferation and viability were examined by 3-(4,5)-dimethylthiazol(-z-y1)-3,5-diphenyl tetrazoliumbromide (MTT assay) and colony formation assay. Cell apoptosis and cell cycle distribution were detected by flow cytometry. Expressions of p53, p21, BAX were assessed by Western blotting. CRC cells transfected with lncRNA-shRNA were injected into nude mice to identify the role of SNHG1 on tumorigenesis in vivo. SNHG1 expression level was elevated in CRC tissues when compared to adjacent tissues (n=86). SNHG1 knockdown significantly suppressed cell proliferation and viability, while SNHG1 overexpression had the opposite effect. Decreased SNHG1 expression enhanced cell apoptosis and triggered cell cycle arrest in G0/G1 phase, while elevated SNHG1 expression done the opposite. Besides, downregulation of SNHG1 impeded tumorigenesis in vivo. Protein levels of p53 and p53 target genes were affected by SNHG1 in vitro. Our research demonstrated that SNHG1 may participate in controlling CRC proliferation, viability, and apoptosis via modulating p53 partially, which provides potential therapeutic targets for CRC.