Pathophysiological Functions of the lncRNA TUG1

Guo, Chong; Qi, Yuying; Qu, Jiayuan; Gai, Liyue; Shi, Yue; Yuan, Chengfu

doi:10.2174/1381612826666191227154009

Cited by 68 publications

(37 citation statements)

References 130 publications

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“…Taurine-upregulated gene 1 (TUG1) is transcribed from a gene localized on chromosome 22 (22q12.2) and it is able to regulate gene expression through different mechanisms, since it interacts with Polycomb repressor complex and functions in the epigenetic regulation of transcription, but can also function in the cytosol sponging microRNAs [ 37 ]. Interestingly, this latter mechanism has been reported for microRNAs implicated in IL-1β, IL-6, IL-10 and TNFα signaling [ 21 , 22 ], and thus in processes involved in CD pathogenesis.…”

Section: Discussionmentioning

confidence: 99%

“…Indeed, increased NEAT1 expression could also represent a defense mechanism triggered by gluten exposure and IL-15 production. In fact, the modulation of the expression of NEAT1 or TUG1 has been reported by various groups as part of a protective response to different stimuli [ 19 , 37 ]. NEAT1 increases after the induction of oxidative stress in HUVEC cells, and this process in mediated by P53 activation [ 39 ].…”

Section: Discussionmentioning

confidence: 99%

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Gliadin, through the Activation of Innate Immunity, Triggers lncRNA NEAT1 Expression in Celiac Disease Duodenal Mucosa

Gnodi

Mancuso

Elli

et al. 2021

IJMS

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Celiac disease (CD) is an autoimmune enteropathy arising in genetically predisposed subjects exposed to gluten, which activates both innate and adaptive immunity. Although the pathogenesis is common to all patients, the clinical spectrum is quite variable, and differences could be explained by gene expression variations. Among the factors able to affect gene expression, there are lncRNAs. We evaluated the expression profile of 87 lncRNAs in CD vs. healthy control (HC) intestinal biopsies by RT-qPCR array. Nuclear enriched abundant transcript 1 (NEAT1) and taurine upregulated gene 1 (TUG1) were detected as downregulated in CD patients at diagnosis, but their expression increased in biopsies of patients on a gluten-free diet (GFD) exposed to gluten. The increase in NEAT1 expression after gluten exposure was mediated by IL-15 and STAT3 activation and binding to the NEAT1 promoter, as demonstrated by gel shift assay. NEAT1 is localized in the nucleus and can regulate gene expression by sequestering transcription factors, and it has been implicated in immune regulation and control of cell proliferation. The demonstration of its regulation by gluten thus also supports the role of lncRNAs in CD and prompts further research on these RNAs as gene expression regulators.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Gliadin, through the Activation of Innate Immunity, Triggers lncRNA NEAT1 Expression in Celiac Disease Duodenal Mucosa

Gnodi

Mancuso

Elli

et al. 2021

IJMS

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“…While some studies have shown that lncRNAs can play opposing roles and behave like oncogenes or tumor-suppressor genes during tumorigenesis, there is still no consensus about the biologic implications of these non-coding transcripts in the clinical setting (3). Prior studies have demonstrated the significant roles that lncRNAs play in fundamental cellular functions, such as pre-transcription, post-transcription, cell proliferation, invasion, differentiation, apoptosis, and migration (4). Increasing evidence suggests that lncRNAs also play a role in regulating cellular functionality and pathogenesis in TC (5).…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA signatures as predictors of prognosis in thyroid cancer: a narrative review

Zhao¹,

Souza²,

Kumar³

et al. 2021

Ann Transl Med

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Thyroid cancer (TC) is the most common endocrine malignancy, with high incidence rates in recent decades. Most TC cases have good prognoses, but a high risk of recurrence and metastases poses challenges, especially for patients with high-risk factors. Currently used prognostic markers for TC involve a combination of genetic factors and overexpressed proteins. Long non-coding RNAs (lncRNAs) regulate several integral biologic processes by playing key roles in the transcription of several downstream targets maintaining cellular behavior. Prior studies have revealed that lncRNAs promote tumor cell proliferation, invasion, metastasis, and angiogenesis, making them important targets for therapeutic intervention in cancer.While the exact molecular mechanisms underlying the role of lncRNAs in modulating TC progression and recurrence is still unclear, it is important to note that some lncRNAs are upregulated in certain cancers, while others are downregulated. In the present study, we review several key lncRNAs, their association with cancer progression, and the important roles they may play as tumor suppressors or tumor promoters in tumorigenesis. We discuss the potential mechanisms of lncRNA-mediated pathogenesis that can be targeted for the treatment of TC, the existing and potential benefits of using lncRNAs as diagnostic and prognostic measures for cancer detection, and tumor burden in patients.

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“…Increasing evidence indicates that lncRNAs possess various regulatory functions in cancer progression, including proliferation, migration, and invasion [ 7 ]. lncRNA taurine upregulated gene 1 (TUG1) is one of the first identified lncRNAs associated with human diseases [ 8 ]. For example, TUG1 promotes cell proliferation and inhibits apoptosis by targeting AURKA in epithelial ovarian cancer [ 9 ].…”

Section: Introductionmentioning

confidence: 99%

LncRNA-TUG1 promotes the progression of infantile hemangioma by regulating miR-137/IGFBP5 axis

2021

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Background Previous studies indicated that lncRNA taurine upregulated gene 1 (TUG1) played essential roles in human cancers. This study aimed to investigate its function in infantile hemangioma (IH). Methods A total of 30 pairs of clinical infantile specimens were used in this study. The expression of TUG1 in IH tissues was assessed by quantitative reverse transcriptase PCR (qRT-PCR). Two short hairpin RNA targeting TUG1 (sh-TUG1-1 and sh-TUG1-2) were transfected into hemangioma-derived endothelial cells, HemECs, to block its expression. The effects of TUG1 on HemECs were evaluated by Cell Counting Kit-8 (CCK-8), colony formation assay, wound healing assay, and Transwell assay. The underlying molecular mechanism of TUG1 was investigated by Starbase prediction and luciferase reporter assay and further determined by loss- and gain-of-function approaches. In addition, the role of TUG1 on tumorigenesis of HemECs was confirmed in an in vivo mouse model. Results TUG1 was significantly upregulated in infant hemangioma tissues compared with normal adjacent subcutaneous tissues. The loss- and gain-of-function approaches indicated that TUG1 overexpression promoted proliferation, migration, and invasion of HemECs in vitro, and TUG1 knockdown inhibited the tumorigenesis of HemECs in vivo. Specifically, TUG1 could compete with IGFBP5 for miR137 binding. Rescue experiments further confirmed the role of the TUG1/miR137/IGFBP5 axis in HemECs. Conclusion TUG1 was closely associated with the progression of IH by regulating the miR-137/IGFBP5 axis, which might be a potential target for IH treatment.

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Pathophysiological Functions of the lncRNA TUG1

Cited by 68 publications

References 130 publications

Gliadin, through the Activation of Innate Immunity, Triggers lncRNA NEAT1 Expression in Celiac Disease Duodenal Mucosa

Gliadin, through the Activation of Innate Immunity, Triggers lncRNA NEAT1 Expression in Celiac Disease Duodenal Mucosa

Long non-coding RNA signatures as predictors of prognosis in thyroid cancer: a narrative review

LncRNA-TUG1 promotes the progression of infantile hemangioma by regulating miR-137/IGFBP5 axis

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