SNHG7 Facilitates Glioblastoma Progression by Functioning as a Molecular Sponge for MicroRNA-449b-5p and Thereby Increasing MYCN Expression

Chen, Yaogang; Yuan, Shaoyong; Ning, Tieying; Xu, Hongbo; Guan, Bo

doi:10.1177/1533033820945802

Cited by 7 publications

(3 citation statements)

References 41 publications

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“…Chen et al found that the expression of SNHG7 was signi cantly increased in glioblastoma and could be used as a molecular sponge to negatively regulate the expression of miR-449b-5p. At this time, the expression of MYCN protein increased and reversed the antitumour effect of miR-449b-5p, thus promoting the proliferation, migration, and invasion of glioblastoma [44]. In another study, Wang et al found that SNHG7 was upregulated in non-small-cell lung cancer (NSCLC) and played an oncogenic role in their experiment.…”

Section: Discussionmentioning

confidence: 96%

The Prognostic Value of Long Non-Coding RNA SNHG7 in Human Cancer: A Meta-Analysis

Yuan

Huang

et al. 2022

CPB

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Background: The long non-coding RNA SNHG7 is upregulated in many types of cancer and plays a role as an oncogene. However, its overall predictive ability in human cancer prognosis has not been assessed using existing databases. Therefore, further study of its prognostic value and clinical significance in human malignancies is warranted. Methods: We systematically collected relevant literature from multiple electronic document databases about the relationship between SNHG7 expression level and prognosis in patients with solid cancers. We further screened them for eligibility. Pooled hazard ratios (HRs) with 95% confidence intervals (CIs) were used to assess the prognostic value. Odds ratios (ORs) and their 95% CIs were collected to evaluate the relationship between the expression of SNHG7 and clinicopathological features, including lymph node metastasis (LNM), tumour size, tumour node metastasis (TNM) stage and histological grade. Results: Fourteen original studies involving 971 patients were enrolled strictly following the inclusion and exclusion criteria. The meta-analysis showed that SNHG7 expression was significantly correlated with poor overall survival (HR = 1.93, 95% CI: 1.64–2.26, p<0.001) in human cancer patients. In addition, the pooled OR indicated that overexpression of SNHG7 was associated with earlier LNM (OR = 1.83, 95% CI: 1.44–2.32; P <0.001), and advanced TNM stage (OR = 1.82, 95% CI: 1.44–2.30; P <0.001).Meanwhile, there was no significant heterogeneity between the selected studies, proving the reliability of the meta-analysis results. Conclusions: High SNHG7 expression may predict poor oncological outcomes in patients with multiple human cancers, which could be a novel prognostic biomarker of unfulfilled clinicopathological features. However, further high-quality studies are needed to verify and strengthen the clinical value of SNHG7 in different types of cancer.

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Section: Discussionmentioning

confidence: 96%

The Prognostic Value of Long Non-Coding RNA SNHG7 in Human Cancer: A Meta-Analysis

Yuan

Huang

et al. 2022

CPB

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“…Additionally, inhibition of miR-5095 in A172 and U-87 MG cells increased the expression of CTNNB1, the gene encoding β-catenin ( 72 ). More recently, Chen et al reported that SNHG7 acts as a miRNA sponge by reducing miRNA-449b-5p levels, increasing MYCN (a miRNA-449b-5p target gene), and promoting GBM progression ( 73 ). In other studies, Han et al reported that the Wnt/β-catenin signaling pathway in GBM is inhibited by the lncRNA MIR22HG through the loss of miR-22-3p and miR-22-5p ( 74 ).…”

Section: Deregulation Of Non-coding Rnas In Gbmmentioning

confidence: 99%

Targeting Non-coding RNA for Glioblastoma Therapy: The Challenge of Overcomes the Blood-Brain Barrier

Sharma

Calderón

Vivas‐Mejía

2021

Front. Med. Technol.

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Glioblastoma (GBM) is the most malignant form of all primary brain tumors, and it is responsible for around 200,000 deaths each year worldwide. The standard therapy for GBM treatment includes surgical resection followed by temozolomide-based chemotherapy and/or radiotherapy. With this treatment, the median survival rate of GBM patients is only 15 months after its initial diagnosis. Therefore, novel and better treatment modalities for GBM treatment are urgently needed. Mounting evidence indicates that non-coding RNAs (ncRNAs) have critical roles as regulators of gene expression. Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) are among the most studied ncRNAs in health and disease. Dysregulation of ncRNAs is observed in virtually all tumor types, including GBMs. Several dysregulated miRNAs and lncRNAs have been identified in GBM cell lines and GBM tumor samples. Some of them have been proposed as diagnostic and prognostic markers, and as targets for GBM treatment. Most ncRNA-based therapies use oligonucleotide RNA molecules which are normally of short life in circulation. Nanoparticles (NPs) have been designed to increase the half-life of oligonucleotide RNAs. An additional challenge faced not only by RNA oligonucleotides but for therapies designed for brain-related conditions, is the presence of the blood-brain barrier (BBB). The BBB is the anatomical barrier that protects the brain from undesirable agents. Although some NPs have been derivatized at their surface to cross the BBB, optimal NPs to deliver oligonucleotide RNA into GBM cells in the brain are currently unavailable. In this review, we describe first the current treatments for GBM therapy. Next, we discuss the most relevant miRNAs and lncRNAs suggested as targets for GBM therapy. Then, we compare the current drug delivery systems (nanocarriers/NPs) for RNA oligonucleotide delivery, the challenges faced to send drugs through the BBB, and the strategies to overcome this barrier. Finally, we categorize the critical points where research should be the focus in order to design optimal NPs for drug delivery into the brain; and thus move the Oligonucleotide RNA-based therapies from the bench to the clinical setting.

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“…Small nucleolar RNA host gene 7 (SNHG7) is a newly identified lncRNA, which located on chromosome 9q34.3 and has a full length of 984 bp. It has been confirmed to be an oncogene in multiple tumors including glioblastoma, lung cancer, breast cancer, and hepatocellular carcinoma (9)(10)(11)(12). In non-small cell lung cancer, SNHG7 can inhibit microRNA (miRNA/miR)-181a-5p via the Akt/mTOR signaling, and facilitate cell proliferation, migration, and invasion (9).…”

Section: Original Articlementioning

confidence: 99%

Long non-coding RNA small nucleolar RNA host gene 7 facilitates the proliferation, migration, and invasion of esophageal cancer cells by regulating microRNA-625

Wang

Bao²,

Wan

et al. 2021

J Gastrointest Oncol

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Background: Esophageal cancer (EC) is a highly aggressive malignant tumor, of which esophageal squamous cell carcinoma (ESCC) constitutes the main subtype. Long non-coding RNA (lncRNA) small nucleolar RNA host gene 7 (SNHG7) has been extensively studied in many tumors and has been confirmed to be an oncogene; however, it has yet to be investigated in an ESCC study. Therefore, this study intended to uncover the role of SNHG7 in ESCC.Methods: Quantitative real-time polymerase chain reaction was applied to measure the expression levels of SNHG7 and miR-625 in ESCC tumor tissues and cell lines. Cell Counting Kit-8 assay, 5-Ethynyl-2'deoxyuridine assay, scratch assay, and Transwell assay were conducted to assess the proliferation, migration, and invasion ESCC cell. We verified the interaction between SNHG7 and miR-625 by performing the dual luciferase reporter gene experiment.Results: Compared to that in adjacent normal tissues and HET1A cell lines, the expression level of SNHG7 in ESCC tumor tissues and ESCC cell lines was up-regulated, while the expression level of miR-625 was down-regulated. ESCC cell proliferation, migration, and invasion were significantly promoted by SNHG7 overexpression but inhibited by silencing of SNHG7. Further, luciferase reporter gene experiments confirmed that SNHG7 interacted with miR-625, and rescue experiments showed that SNHG7 promoted the malignant phenotype by inhibiting miR-625.Conclusions: SNHG7 is up-regulated in ESCC tumor tissues and cell lines, while miR-625 is expressed at a low level. SNHG7 is able to facilitate the proliferation, migration, and invasion of ESCC cells by targeting miR-625.

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SNHG7 Facilitates Glioblastoma Progression by Functioning as a Molecular Sponge for MicroRNA-449b-5p and Thereby Increasing MYCN Expression

Cited by 7 publications

References 41 publications

The Prognostic Value of Long Non-Coding RNA SNHG7 in Human Cancer: A Meta-Analysis

The Prognostic Value of Long Non-Coding RNA SNHG7 in Human Cancer: A Meta-Analysis

Targeting Non-coding RNA for Glioblastoma Therapy: The Challenge of Overcomes the Blood-Brain Barrier

Long non-coding RNA small nucleolar RNA host gene 7 facilitates the proliferation, migration, and invasion of esophageal cancer cells by regulating microRNA-625

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