New insights into long noncoding RNAs and their roles in glioma

Peng, Zixuan; Liu, Changhong; Wu, Minghua

doi:10.1186/s12943-018-0812-2

Cited by 324 publications

(270 citation statements)

References 79 publications

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“…The molecular mechanisms mediating the roles of lncRNAs are complex and diverse . As a class of regulatory RNAs, lncRNAs directly bind proteins, DNAs, mRNAs and/or microRNAs .…”

Section: Discussionmentioning

confidence: 99%

Long non‐coding RNA LINC00526 represses glioma progression via forming a double negative feedback loop with AXL

Yan

et al. 2019

J Cellular Molecular Medi

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Glioma is the most common primary intracranial carcinoma with extremely poor prognosis. The significances of long non‐coding RNA (lncRNA) involved in glioma have been started revealed. However, the expression, roles and molecular mechanisms of most lncRNAs in glioma are still unknown. In this study, we identified a novel lncRNA LINC00526, which is significantly low expressed in glioma. Low expression of LINC00526 is correlated with aggravation and poor survival in glioma. Functional assays revealed that ectopic expression of LINC00526 inhibits glioma cell proliferation, migration, and invasion. LINC00526 silencing promotes glioma cell proliferation, migration and invasion. Mechanistically, we found that LINC00526 directly interacts with EZH2, represses the binding of EZH2 to AXL promoter, attenuates the transcriptional activating roles of EZH2 on AXL , and therefore represses AXL expression. Via repressing AXL, LINC00526 further represses PI3K/Akt/NF‐κB signalling. Intriguingly, we identified that NFKB1 and NFKB2 directly binds LINC00526 promoter and represses LINC00526 transcription. We further found that via activating NF‐κB signalling, AXL represses LINC00526 transcription. Therefore, LINC00526/EZH2/AXL/PI3K/Akt/NF‐κB form a feedback loop in glioma. Analysis of the TCGA data revealed that the expression of LINC00526 is inversely correlated with that of AXL in glioma tissues. In addition, functional rescue assays revealed that the tumour suppressive roles of LINC00526 are dependent on the negative regulation of AXL. Collectively, our data identified LINC00526 as a tumour suppressor in glioma via forming a double negative feedback loop with AXL. Our data also suggested LINC00526 as a potential prognostic biomarker and therapeutic candidate for glioma.

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“…The molecular mechanisms mediating the roles of lncRNAs are complex and diverse . As a class of regulatory RNAs, lncRNAs directly bind proteins, DNAs, mRNAs and/or microRNAs .…”

Section: Discussionmentioning

confidence: 99%

Long non‐coding RNA LINC00526 represses glioma progression via forming a double negative feedback loop with AXL

Yan

et al. 2019

J Cellular Molecular Medi

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“…Increasing evidence shows that aberrant expression profiles of lncRNAs in clinical glioma specimens have been observed to correlate with malignancy grade and histological differentiation . Furthermore, lncRNAs have been found to be implicated in the onset and progression of glioma through the regulation of stemness, proliferation, migration, angiogenesis and drug resistance . There is convincing evidence that lncRNA maternally expressed gene 3 (MEG3) is a novel valuable in glioma .…”

Section: Discussionmentioning

confidence: 99%

“…Glioma is one of the most common types of primary malignant brain tumours, characterized by rapid cell proliferation and angiogenesis . Glioma is classified as several histological subtypes, including astrocytomas, glioblastoma (GBM), oligodendrogliomas and mixed tumours . Currently, standard treatment for glioma is surgical removal, accompanied by radiotherapy and adjuvant chemotherapy .…”

Section: Introductionmentioning

confidence: 99%

ZFAS1 knockdown inhibits viability and enhances cisplatin cytotoxicity by up‐regulating miR‐432‐5p in glioma cells

Yang

Han

Feng

2019

Basic Clin Pharma Tox

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Background Long non‐coding RNA (lncRNA) zinc finger antisense 1 (ZFAS1) is a novel vital oncogenic lncRNA that is dysregulated in various types of cancers, including glioma. According to TargetScan prediction, miR‐432‐5p is a target of ZFAS1. Herein, we aimed to determine whether there was a correlation between ZFAS1 and miR‐432‐5p and to explore their roles in glioma. Methods The expression levels of ZFAS1 and microRNA (miR)‐432‐5p in clinical tissues and cell lines were measured using RT‐qPCR. Cell viability was detected using MTT assay. Cell apoptosis was examined using flow cytometry. The association between ZFAS1 and miR‐432‐5p was confirmed using luciferase reporter and RNA pull‐down assays. Results Zinc finger antisense 1 expression was up‐regulated, while miR‐432‐5p expression was down‐regulated in both glioma tissues and cells. Knockdown of ZFAS1 and miR‐432‐5p overexpression inhibited cell viability and enhanced the chemosensitivity of glioma cells to cisplatin. MiR‐432‐5p was a direct target of ZFAS1 in glioma cells. Inhibition of miR‐432‐5p blocked the effects of ZFAS1 knockdown on cell viability and cisplatin sensitivity. Conclusions Knockdown of ZFAS1 inhibited the viability and enhanced cisplatin sensitivity via targeting miR‐432‐5p in glioma cells.

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“…It is well known that epigenetic alterations or genetic modulation of epigenetic regulators plays important roles in carcinogenesis . Many studies show that the anticancer effect of propofol is potentially due to regulation of the epigenetic pathway in cancer …”

Section: Epigenetic Pathwaysmentioning

confidence: 99%

The mechanism of propofol in cancer development: An updated review

Gao

Guo

et al. 2020

Asia-Pac J Clncl Oncology

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Cancer is a key cause of death worldwide. Despite the development of radiotherapy, chemotherapy and even immunotherapy, surgery remains the standard treatment for cancer patients. Recently, many studies have shown that propofol, a commonly used anesthetic drug, can affect the prognosis of cancer. In this review, we provide an overview of the molecular mechanisms of propofol in the development of cancer. Propofol not only affects epigenetic pathways, such as those involving miRNA, lncRNA and histone acetylation, but also modulates genetic signaling pathways, including the hypoxia, NF‐κB, MAPK, SLUG and Nrf2 pathways. In addition, propofol influences the immune function of patients and impacts the degree of immunosuppression. Furthermore, we briefly summarize the clinical trials on the effect of propofol in cancer development. Ultimately, further studies distinguishing the types of tumors in clinical trials are needed to clarify the correlation between propofol and cancer.

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New insights into long noncoding RNAs and their roles in glioma

Cited by 324 publications

References 79 publications

Long non‐coding RNA LINC00526 represses glioma progression via forming a double negative feedback loop with AXL

Long non‐coding RNA LINC00526 represses glioma progression via forming a double negative feedback loop with AXL

ZFAS1 knockdown inhibits viability and enhances cisplatin cytotoxicity by up‐regulating miR‐432‐5p in glioma cells

The mechanism of propofol in cancer development: An updated review

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