Long noncoding RNA SNHG17 induced by YY1 facilitates the glioma progression through targeting miR-506-3p/CTNNB1 axis to activate Wnt/β-catenin signaling pathway

Li, Huixia; Li, Tianhao; Huang, Dehai; Zhang, Peng

doi:10.1186/s12935-019-1088-3

Cited by 35 publications

(29 citation statements)

References 32 publications

(28 reference statements)

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“…et al, 2018 ; Zhang G. et al, 2018 ). SNHG17 regulates cell functions by acting as a molecular sponge for miRNAs in breast cancer ( Du et al, 2020 ), tongue squamous cell carcinoma ( Liu et al, 2020 ), and glioma ( Li et al, 2020 ). Using bioinformatic analyses, AGO2-RIP, luciferase reporter assays, and RNA pull-down assays, we demonstrated that SNHG17 sponges miR-3180-3p and inhibits its expression.…”

Section: Discussionmentioning

confidence: 99%

Long Non-coding RNA SNHG17 Upregulates RFX1 by Sponging miR-3180-3p and Promotes Cellular Function in Hepatocellular Carcinoma

Zhou²,

Wei

et al. 2021

Front. Genet.

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BackgroundHepatocellular carcinoma (HCC) is one of the most common types of cancer that is associated with poor quality of life in patients and a global health burden. The mechanisms involved in the development and progression of HCC remain poorly understood.MethodsHepatocellular carcinoma human samples and cell lines were subjected to qRT-PCR for expression assessment. CCK-8 assay, Transwell migration and invasion assay, were applied for cell function detection. Animal experiment was used to measure the function of SNHG17 on cell growth in vivo. Western blot was conducted to evaluate the level of EMT in cells. RIP, RNA pull-down and luciferase reporter assays were performed to assess the correlation between SNHG17, miR-3180-3p and RFX1.ResultsOur study demonstrated that SNHG17 was upregulated in HCC human samples and involved cell proliferation, migration, invasion progress. SNHG17 promoted HCC cell growth and metastasis in vivo. Furthermore, we investigated the downstream factor of SNHG17, SNHG17 acted as a molecular sponge for miR-3180-3p, and SNHG17 regulated RFX1 expression via miR-3180-3p. SNHG17 promotes tumor-like behavior in HCC cells via miR-3180-3p/RFX1.ConclusionWe determined RFX1 as the target of miR-3810-3p; SNHG17 enhanced the progression of HCC via the miR-3180-3p/RFX1 axis. Taken together, our findings may provide insight into the molecular mechanism involved in the progression of HCC and develop SNHG17 as a novel therapeutic target against HCC.

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Section: Discussionmentioning

confidence: 99%

Long Non-coding RNA SNHG17 Upregulates RFX1 by Sponging miR-3180-3p and Promotes Cellular Function in Hepatocellular Carcinoma

Zhou²,

Wei

et al. 2021

Front. Genet.

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“…When miR-218 is overexpressed, YY1 is downregulated and the inhibition of the tumor suppressor p53 is nullified ( Gao et al, 2018 ). Additionally, YY1 was shown to upregulate transcription of the long non-coding RNA SNHG17, which activates the Wnt/β-catenin signaling pathway and thus contributes to the proliferation of glioma cells and inhibition of apoptosis ( Li et al, 2020 ).…”

Section: Yy1 In Health and Diseasementioning

confidence: 99%

The Why of YY1: Mechanisms of Transcriptional Regulation by Yin Yang 1

Verheul

Hijfte

Perenthaler

et al. 2020

Front. Cell Dev. Biol.

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First described in 1991, Yin Yang 1 (YY1) is a transcription factor that is ubiquitously expressed throughout mammalian cells. It regulates both transcriptional activation and repression, in a seemingly context-dependent manner. YY1 has a well-established role in the development of the central nervous system, where it is involved in neurogenesis and maintenance of homeostasis in the developing brain. In neurodevelopmental and neurodegenerative disease, the crucial role of YY1 in cellular processes in the central nervous system is further underscored. In this mini-review, we discuss the various mechanisms leading to the transcriptional activating and repressing roles of YY1, including its role as a traditional transcription factor, its interactions with cofactors and chromatin modifiers, the role of YY1 in the non-coding genome and 3D chromatin organization and the possible implications of the phase-separation mechanism on YY1 function. We provide examples on how these processes can be involved in normal development and how alterations can lead to various diseases.

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“…[20,21] For instance, SNHG17, as a sponge of miR-506-3p, was clari ed to upregulate the expression of CTNNB1 in glioma. [22] Furthermore, miR-124-3p is proven to be a sponge of SNHG17 in breast cancer cell lines. [11] In the present experiment, we worked hard to examine whether SNHG17 may also function as a ceRNA to regulate RCC's tumorigenesis and progression.…”

Section: Discussionmentioning

confidence: 99%

LncRNA SNHG17 Promotes Tumor Progression and Predicts Poor Survival in Human Renal Cell Carcinoma via Sponging miR-328-3p

Dong

Liu

et al. 2020

Preprint

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Background: Accumulating data shows that dysregulation of long non-coding RNAs (lncRNAs) are involved in human tumors' occurrence and progression. Small nucleolar RNA host genes (SNHGs) are recently revealed to play a carcinogenic role in various human neoplasms. However, the functions and underlying mechanisms of lncRNA SNHG17 in renal cell carcinoma (RCC) are still elusive.Methods: We analyzed the relationship between SNHG17 expression levels and clinicopathologic characteristics and prognosis in patients with RCC according to TCGA RNA-sequencing data and our cohort data. Loss-of-function and gain-of-function experiments were conducted to examine the biological behaviors of SNHG17 on RCC cell proliferation, migration, invasion, apoptosis, and tumor growth in vivo. The interaction between SNHG17, miR-328-3p, and Histone’s H2A variant (H2AX) was verified by bioinformatics, dual-luciferase reporter gene, and RNA immunoprecipitation (RIP). Results: Highly expressed SNHG17 was evident in RCC tissue samples and cell lines, and SNHG17 overexpression was related to advanced TNM stage and reduced relapse-free and overall survival of patients with RCC. Knockdown of SNHG17 prohibited malignant phenotypes, whereas ectopic SNHG17 expression showed the opposite effects. More importantly, SNHG17 could upregulate the expression of H2AX by acting as a miR-328-3p sponge. In vivo experiments confirmed that SNHG17 promoted the growth of RCC tumors.Conclusion: SNHG17/miR-328-3p/H2AX axis might be involved in RCC progression, which provided a potential therapeutic target for RCC.

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Long noncoding RNA SNHG17 induced by YY1 facilitates the glioma progression through targeting miR-506-3p/CTNNB1 axis to activate Wnt/β-catenin signaling pathway

Cited by 35 publications

References 32 publications

Long Non-coding RNA SNHG17 Upregulates RFX1 by Sponging miR-3180-3p and Promotes Cellular Function in Hepatocellular Carcinoma

Long Non-coding RNA SNHG17 Upregulates RFX1 by Sponging miR-3180-3p and Promotes Cellular Function in Hepatocellular Carcinoma

The Why of YY1: Mechanisms of Transcriptional Regulation by Yin Yang 1

LncRNA SNHG17 Promotes Tumor Progression and Predicts Poor Survival in Human Renal Cell Carcinoma via Sponging miR-328-3p

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