NoncoRNA: a database of experimentally supported non-coding RNAs and drug targets in cancer

Li, Lulu; Wu, Pengfei; Wang, Zhenyu; Meng, Xiangqi; Zha, Caijun; Li, Ziwei; Qi, Tengfei; Zhang, Yangong; Han, Bo; Li, Shupeng; Jiang, Chuanlu; Zhao, Zheng

doi:10.1186/s13045-020-00849-7

Cited by 54 publications

(47 citation statements)

References 10 publications

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“…Additionally, in acute myeloma cell lines, targeting PLK2 by miR-126 induces the downregulation of PLK2 and inhibits cell apoptosis and increases cell viability [14]. Moreover, the same micro-RNA was closely associated with TMZ resistance according to NoncoRNA database [15]. However, the potential function of PLK2 in GBM carcinogenesis and chemoresistance remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Loss of PLK2 induces acquired resistance to temozolomide in GBM via activation of notch signaling

Wahafu

et al. 2020

J Exp Clin Cancer Res

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Background Glioblastoma (GBM) is a lethal type of primary brain tumor with a median survival less than 15 months. Despite the recent improvements of comprehensive strategies, the outcomes for GBM patients remain dismal. Accumulating evidence indicates that rapid acquired chemoresistance is the major cause of GBM recurrence thus leads to worse clinical outcomes. Therefore, developing novel biomarkers and therapeutic targets for chemoresistant GBM is crucial for long-term cures. Methods Transcriptomic profiles of glioblastoma were downloaded from gene expression omnibus (GEO) and TCGA database. Differentially expressed genes were analyzed and candidate gene PLK2 was selected for subsequent validation. Clinical samples and corresponding data were collected from our center and measured using immunohistochemistry analysis. Lentiviral transduction and in vivo xenograft transplantation were used to validate the bioinformatic findings. GSEA analyses were conducted to identify potential signaling pathways related to PLK2 expression and further confirmed by in vitro mechanistic assays. Results In this study, we identified PLK2 as an extremely suppressed kinase-encoding gene in GBM samples, particularly in therapy resistant GBM. Additionally, reduced PLK2 expression implied poor prognosis and TMZ resistance in GBM patients. Functionally, up-regulated PLK2 attenuated cell proliferation, migration, invasion, and tumorigenesis of GBM cells. Besides, exogenous overexpression of PLK2 reduced acquired TMZ resistance of GBM cells. Furthermore, bioinformatics analysis indicated that PLK2 was negatively correlated with Notch signaling pathway in GBM. Mechanically, loss of PLK2 activated Notch pathway through negative transcriptional regulation of HES1 and degradation of Notch1. Conclusion Loss of PLK2 enhances aggressive biological behavior of GBM through activation of Notch signaling, indicating that PLK2 could be a prognostic biomarker and potential therapeutic target for chemoresistant GBM.

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Section: Introductionmentioning

confidence: 99%

Loss of PLK2 induces acquired resistance to temozolomide in GBM via activation of notch signaling

Wahafu

et al. 2020

J Exp Clin Cancer Res

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“…LncRNAs are emerging as important regulators in different disease processes including cancer [34,[38][39][40][41][42]. Recently, growing numbers of lncRNAs have been found to be dysregulated in glioma.…”

Section: Discussionmentioning

confidence: 99%

LncRNA BCYRN1 inhibits glioma tumorigenesis by competitively binding with miR-619-5p to regulate CUEDC2 expression and the PTEN/AKT/p21 pathway

Niu

Zhang

et al. 2020

Oncogene

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Glioma is the most common malignant tumor in the central nervous system. Altered long noncoding RNAs (lncRNAs) are playing regulatory roles in physiological and pathogenic processes in cancer. Here, we uncovered a differentially expressed lncRNA called brain cytoplasmic RNA 1 (BCYRN1), and elucidated its function and molecular mechanism in the progression and development of glioma. Three fresh tumor tissues from glioma patients and three normal brain tissues from craniocerebral trauma patients were prepared for high-throughput RNA sequencing. Differential RNA transcripts and BCYRN1 were identified by RT-qPCR in glioma samples and controls. CCK-8, colony formation assays, flow cytometry, TUNEL assays, cell migration assays, wound-healing assays, and xenograft model were established to investigate the biological function of BCYRN1 both in vitro and in vivo. Various bioinformatics analysis, dual-luciferase reporter assays, biotinylated RNA pulldown assays, and rescue experiments were conducted to reveal the underlying mechanisms of competitive endogenous RNAs (ceRNAs). 183 lncRNAs were identified with significant dysregulation in glioma and randomly selected differential RNAs were further confirmed by RT-qPCR. Among them, BCYRN1 was the most downregulated lncRNA, and its low expression positively correlated with glioma progression. Functionally, BCYRN1 overexpression inhibited cell proliferation, migration in glioma cell lines, whereas BCYRN1 depletion resulted in the opposite way. MiR-619-5p was further confirmed as the direct target of BCYRN1. Mechanistically, miR-619-5p specifically targeted the CUE domain containing protein 2 (CUEDC2), and BCYRN1/miR-619-5p suppressed glioma tumorigenesis by inactivating PTEN/AKT/p21 pathway in a CUEDC2-dependent manner. Overall, our data presented that the reduced expression of BCYRN1 was associated with poor patient outcome in glioma. BCYRN1 functioned as a ceRNA to inhibit glioma progression by sponging miR-619-5p to regulate CUEDC2 expression and PTEN/AKT/p21 pathway. Our results indicated that BCYRN1 exerted tumor suppressor potential and might be a candidate in the diagnosis and treatment of glioma.

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“…The diverse ncRNA–disease associations from 17 related experimentally validate databases ( 16–32 ) and 14 computationally predicted algorithms ( 31–44 ) were also integrated ( Supplemental Table S1 ). In extension, drug-related information was obtained from four databases: ncDR ( 45 ), NoncoRNA ( 46 ), NRDTD ( 47 ) and RNAInter ( 48 ), ncRNA subcellular localizations were obtained from RNALocate ( 15 ) and interactions from RNAInter ( 48 ).…”

Section: Data Collection and Orgnizationmentioning

confidence: 99%

MNDR v3.0: mammal ncRNA–disease repository with increased coverage and annotation

Lin

Cui

Zheng

et al. 2020

Nucleic Acids Research

108

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Many studies have indicated that non-coding RNA (ncRNA) dysfunction is closely related to numerous diseases. Recently, accumulated ncRNA–disease associations have made related databases insufficient to meet the demands of biomedical research. The constant updating of ncRNA–disease resources has become essential. Here, we have updated the mammal ncRNA–disease repository (MNDR, http://www.rna-society.org/mndr/) to version 3.0, containing more than one million entries, four-fold increment in data compared to the previous version. Experimental and predicted circRNA–disease associations have been integrated, increasing the number of categories of ncRNAs to five, and the number of mammalian species to 11. Moreover, ncRNA–disease related drug annotations and associations, as well as ncRNA subcellular localizations and interactions, were added. In addition, three ncRNA–disease (miRNA/lncRNA/circRNA) prediction tools were provided, and the website was also optimized, making it more practical and user-friendly. In summary, MNDR v3.0 will be a valuable resource for the investigation of disease mechanisms and clinical treatment strategies.

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NoncoRNA: a database of experimentally supported non-coding RNAs and drug targets in cancer

Cited by 54 publications

References 10 publications

Loss of PLK2 induces acquired resistance to temozolomide in GBM via activation of notch signaling

Loss of PLK2 induces acquired resistance to temozolomide in GBM via activation of notch signaling

LncRNA BCYRN1 inhibits glioma tumorigenesis by competitively binding with miR-619-5p to regulate CUEDC2 expression and the PTEN/AKT/p21 pathway

MNDR v3.0: mammal ncRNA–disease repository with increased coverage and annotation

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