Long Noncoding RNA DRAIC Inhibits Prostate Cancer Progression by Interacting with IKK to Inhibit NF-κB Activation

Saha, Shekhar; Kiran, Manjari; Kuscu, Canan; Chatrath, Ajay; Wotton, David; Mayo, Marty W.; Dutta, Anindya

doi:10.1158/0008-5472.can-19-3460

Cited by 57 publications

(54 citation statements)

References 63 publications

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“…In contrast, several NF-κB-related lncRNAs are down-regulated and function as tumor suppressors during cancer progression. For example, Saha et al [65] reported that the downregulated RNA in cancer (DRAIC) interacted with the subunits of the IκB kinase (IKK) complex and subsequently inhibited prostate cancer progression by repressing IκBα phosphorylation and NF-κB activation. Additionally, the lncRNA keratin 19 pseudogene 3 (KRT19P3) inhibited gastric cancer cell growth and metastasis by modulating IκBα deubiquitination and inactivating NF-κB signalling [66].…”

Section: Nf-κbmentioning

confidence: 99%

LncRNA‐mediated posttranslational modifications and reprogramming of energy metabolism in cancer

Tan

Lin

et al. 2020

Cancer Communications

428

223

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Altered metabolism is a hallmark of cancer, and the reprogramming of energy metabolism has historically been considered a general phenomenon of tumors. It is well recognized that long noncoding RNAs (lncRNAs) regulate energy metabolism in cancer. However, lncRNA-mediated posttranslational modifications and metabolic reprogramming are unclear at present. In this review, we summarized the current understanding of the interactions between the alterations in cancer-associated energy metabolism and the lncRNA-mediated posttranslational modifications of metabolic enzymes, transcription factors, and other proteins involved in metabolic pathways. In addition, we discuss the mechanisms through which these interactions contribute to tumor initiation and progression, and the key roles and clinical significance of functional lncRNAs. We believe that an in-depth understanding of lncRNA-mediated cancer metabolic

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Section: Nf-κbmentioning

confidence: 99%

LncRNA‐mediated posttranslational modifications and reprogramming of energy metabolism in cancer

Tan

Lin

et al. 2020

Cancer Communications

428

223

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“…We noticed that lncRNA DRAIC had the most significant effect in predicting the prognosis of patients after receiving radiotherapy; lncRNA DRAIC has been shown to inhibit the progression of prostate cancer by interacting with IkB kinase (IKK) and inhibiting NF-kB activity (43). Activation of NF-kB is associated with the radiosensitivity of gliomas (44)(45)(46).…”

Section: Discussionmentioning

confidence: 99%

Developing a lncRNA Signature to Predict the Radiotherapy Response of Lower-Grade Gliomas Using Co-expression and ceRNA Network Analysis

Cai

et al. 2021

Front. Oncol.

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BackgroundLower-grade glioma (LGG) is a type of central nervous system tumor that includes WHO grade II and grade III gliomas. Despite developments in medical science and technology and the availability of several treatment options, the management of LGG warrants further research. Surgical treatment for LGG treatment poses a challenge owing to its often inaccessible locations in the brain. Although radiation therapy (RT) is the most important approach in this condition and offers more advantages compared to surgery and chemotherapy, it is associated with certain limitations. Responses can vary from individual to individual based on genetic differences. The relationship between non-coding RNA and the response to radiation therapy, especially at the molecular level, is still undefined.MethodsIn this study, using The Cancer Genome Atlas dataset and bioinformatics, the gene co-expression network that is involved in the response to radiation therapy in lower-grade gliomas was determined, and the ceRNA network of radiotherapy response was constructed based on three databases of RNA interaction. Next, survival analysis was performed for hub genes in the co-expression network, and the high-efficiency biomarkers that could predict the prognosis of patients with LGG undergoing radiotherapy was identified.ResultsWe found that some modules in the co-expression network were related to the radiotherapy responses in patients with LGG. Based on the genes in those modules and the three databases, we constructed a ceRNA network for the regulation of radiotherapy responses in LGG. We identified the hub genes and found that the long non-coding RNA, DRAIC, is a potential molecular biomarker to predict the prognosis of radiotherapy in LGG.

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“…Based on the differential expression of DRAIC in GC and NC tissues and its potential role in several malignant tumors [10][11][12][13][14][15][16][17], we decided to explore the relationship between DRAIC/ NFRKB and malignant phenotype of GC cells. It was found that DRAIC can restrain the proliferation abilities of HGC-27 and MKN45 cells ( Fig.…”

Section: Biological Effects Of Oedraic and Rescued By Oenfrkb On Gc Cmentioning

confidence: 99%

“…The lncRNA DRAIC gene, which is located on human chromosome 15q23, was reported as a novel tumor regulator in several cancers recently, but it seemed to exhibit different biological effects in cancer cells from different sources [10][11][12][13][14][15][16][17]. On account of the potential value of DRAIC as a GC marker and target, we intended to reveal the expression characteristics and precise mechanism of DRAIC.…”

Section: Biological Effects Of Shdraic On Gc Cellsmentioning

confidence: 99%

“…In 2015, lncRNA Downregulated RNA in cancer (DRAIC) was firstly reported as a target gene of FOXA1 and NKX3-1 to inhibit the ability of transition from an androgendependent (AD) to a castration-resistance state, epithelial-mesenchymal transition (EMT) and metastasis of prostate cancer cells, and TCGA database analysis showed that its expression was closely related to the survival rate of patients with malignant tumors such as GC, lung cancer and hepatocellular carcinoma [10,11]. In addition, high expression of nuclear factor kappa-B (NF-κb) was found in the tumor tissues with inferior DRAIC, and vitro and vivo studies verified that DRAIC could inhibit activation of NF-κb and prostate cancer progressions via binding to subunits of the IκB kinase (IKK) complex [12]. Meanwhile, RNA sequencing (RNA-seq) identified strong downregulation of DRAIC in retinoblastoma compared with that in normal retina, and restoring DRAIC significantly slowed the growth of the Y79 retinoblastoma cell line [13].…”

Section: Introductionmentioning

confidence: 99%

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LncRNA DRAIC inhibits proliferation and metastasis of gastric cancer cells through interfering with NFRKB deubiquitination mediated by UCHL5

Zhang

Kuang

et al. 2020

Cell Mol Biol Lett

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Background: Long non-coding RNA (lncRNA) as a widespread and pivotal epigenetic molecule participates in the occurrence and progression of malignant tumors. DRAIC, a kind of lncRNA whose coding gene location is on 15q23 chromatin, has been found to be weakly expressed in a variety of malignant tumors and acts as a suppressor, but its characteristics and role in gastric cancer (GC) remain to be elucidated. Methods: Sixty-seven primary GC tissues and paired paracancerous normal tissues were collected. Bioinformatics is used to predict the interaction molecules of DRAIC. DRAIC and NFRKB were overexpressed or interfered exogenously in GC cells by lentivirus or transient transfection. Quantitative real-time PCR (qPCR) and western blotting were used to evaluate the expression of DRAIC, UCHL5 and NFRKB. The combinations of DRAIC and NFRKB or UCHL5 and NFRKB were verified by RNA-IP and Co-IP assays. Ubiquitination-IP and the treatment of MG132 and CHX were used to detect the ubiquitylation level of NFRKB. The CCK-8 and transwell invasion and migration assays measured the proliferation, migration and invasion of GC cells. Results: DRAIC is down-regulated in GC tissues and cell lines while its potential interacting molecules UCHL5 and NFRKB are up-regulated, and DRAIC is positively correlated with NFRKB protein instead of mRNA. Lower DRAIC and higher UCHL5 and NFRKB indicated advanced progression of GC patients. DRAIC could increase NFRKB protein significantly instead of NFRKB mRNA and UCHL5, and bind to UCHL5. DRAIC combined with UCHL5 and attenuated binding of UCHL5 and NFRKB, meanwhile promoting the degradation of NFRKB via ubiquitination, and then inhibited the proliferation and metastasis of GC cells, which can be rescued by oeNFRKB. Conclusion: DRAIC suppresses GC proliferation and metastasis via interfering with the combination of UCHL5 and NFRKB and mediating ubiquitination degradation.

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Long Noncoding RNA DRAIC Inhibits Prostate Cancer Progression by Interacting with IKK to Inhibit NF-κB Activation

Cited by 57 publications

References 63 publications

LncRNA‐mediated posttranslational modifications and reprogramming of energy metabolism in cancer

LncRNA‐mediated posttranslational modifications and reprogramming of energy metabolism in cancer

Developing a lncRNA Signature to Predict the Radiotherapy Response of Lower-Grade Gliomas Using Co-expression and ceRNA Network Analysis

LncRNA DRAIC inhibits proliferation and metastasis of gastric cancer cells through interfering with NFRKB deubiquitination mediated by UCHL5

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