Long non-coding RNA NORAD induces cell proliferation and migration in prostate cancer

Zhang, Haiyan; Guo, Haixiang

doi:10.1177/0300060519862076

Cited by 17 publications

(16 citation statements)

References 21 publications

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“…Another research revealed that NORAD was upregulated in colorectal cancer tissues, and NORAD inhibition induced apoptosis and constrained invasion, migration, and proliferation of colorectal cancer cells [ 31 ]. Zhang et al stated that NORAD exhaustion constrained migration, proliferation, and accelerated apoptosis of PCa cells [ 13 ]. We also observed that NORAD expression was boosted in PCa tissues and cells.…”

Section: Discussionmentioning

confidence: 99%

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Long non-coding RNA NORAD exhaustion represses prostate cancer progression through inhibiting TRIP13 expression via competitively binding to miR-495-3p

2020

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Background: Prostate cancer (PCa) is a malignant heterogeneous tumor that threatens men's health. Long noncoding RNA activated by DNA damage (NORAD) and microRNA-495-3p (miR-495-3p) have been revealed to be concerned with the tumorigenesis and progression of diverse cancers. Nevertheless, the regulatory mechanism between NORAD and miR-495-3p in PCa is unclear. Methods: The expression of NORAD, miR-495-3p, and thyroid hormone receptor interactor 13 (TRIP13) mRNA was detected with quantitative real-time polymerase chain reaction (qRT-PCR). The levels of Bcl-2, Bax, Cleaved-casp-3, TRIP13, cyclin D1, and PCNA were detected through western blot analysis. The proliferation, apoptosis, migration, and invasion of PCa cells were assessed through 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT), flow cytometry, or transwell assays. The relationship between NORAD or TRIP13 and miR-495-3p was confirmed via dualluciferase reporter, RIP, or RNA pull-down assays. Results: NORAD and TRIP13 were upregulated while miR-495-3p was downregulated in PCa tissues and cells. Both NORAD silencing and miR-495-3p upregulation accelerated cell apoptosis and curbed cell proliferation, migration, and invasion in PCa cells. Also, NORAD silencing repressed tumor growth in vivo. Notably, NORAD modulated TRIP13 expression by competitively binding to miR-495-3p. Furthermore, miR-495-3p repression reversed NORAD knockdown-mediated effects on the malignant behaviors of PCa cells. Moreover, TRIP13 enhancement overturned the effects of miR-495-3p overexpression on the proliferation, apoptosis, migration, and invasion of PCa cells. Conclusion: NORAD depletion inhibited PCa advancement via the miR-495-3p/ TRIP13 axis, which provided a potential tactic for PCa treatment.

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Section: Discussionmentioning

confidence: 99%

“…Also, NORAD depletion repressed epithelial ovarian cancer advancement [12]. Furthermore, NORAD was concerned with the tumorigenesis of PCa [13]. Nevertheless, the regulatory mechanism of NORAD in PCa progression has been not been well explained.…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA NORAD exhaustion represses prostate cancer progression through inhibiting TRIP13 expression via competitively binding to miR-495-3p

2020

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“…Previous studies in the last several decades have indicated that NORAD serves a pivotal regulator in the occurrence and progression of a variety of malignancies, including gastric cancer, prostate cancer, and osteosarcoma [ 10 , 15 , 16 ]. Overexpression of NORAD is closely related to poor prognosis in various patients with cancer, such as esophageal squamous cell carcinoma, gastric cancer, and ovarian cancer [ 17 – 19 ].…”

Section: Discussionmentioning

confidence: 99%

Silencing of Long Non-Coding RNA (LncRNA) Non-Coding RNA Activated by DNA Damage (NORAD) Inhibits Proliferation, Invasion, Migration, and Promotes Apoptosis of Glioma Cells via Downregulating the Expression of AKR1B1

et al. 2020

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Background We aimed to investigate the functions of long non-coding RNA (lncRNA) non-coding RNA activated by DNA damage (NORAD) in glioma and identify the potential mechanisms. Material/Methods The expression of NORAD and AKR1B1 in human glioma cell lines were examined using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Then, cell proliferation, invasion, and migration were tested by Cell Counting Kit-8 (CCK-8), colony formation assay, Transwell, and scratch wound healing assay after NORAD silencing. Meanwhile, western blotting was utilized to measure the expression of migration-related proteins. Apoptosis of glioma cells was detected using flow cytometry and apoptosis-related proteins expression was determined. Moreover, the correlation between NORAD and AKR1B1 was verified by RNA-binding protein immunoprecipitation (RIP assay). After co-transfection with AKR1B1 overexpressed plasmid and NORAD siRNA, cell proliferation, invasion, migration, and apoptosis were examined again. Furthermore, the expression of proteins in extracellular signal-regulated kinase (ERK) signaling was tested using western blotting. Results The results revealed that NORAD and AKR1B1 were highly expressed in glioma cells. NORAD silencing inhibited proliferation, invasion and migration but promoted apoptosis of glioma cells, accompanied by the expression changes of migration- and apoptosis-related proteins. However, after co-transfection with AKR1B1 pcDNA3.1 in NORAD silencing cells, the effects of NORAD silencing on proliferation, invasion, migration, and apoptosis were attenuated. Consistently, the expression of phosphorylated ERK (p-ERK) was decreased after NORAD silencing, which were reversed following AKR1B1 overexpression. Conclusions These findings demonstrated that NORAD silencing suppressed proliferation, invasion, and migration and boosted apoptosis of glioma cells via downregulating the AKR1B1 expression, which may provide a potential therapeutic target for glioma treatment.

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“…It has been reported that some lncRNAs contribute to DDP resistance in NSCLC (Hu et al 2017;Tian et al 2019). Recently, noncoding RNA activated by DNA damage (NORAD) has attracted attention because of its promoting role in tumour progression (Liu et al 2016;Li et al 2018a;Zhang et al 2019). Zhang et al have shown that NORAD promotes colorectal tumour growth by inhibiting miR-202-5p (Zzhang et al 2018).…”

Section: Introductionmentioning

confidence: 99%

LncRNA NORAD/miR-202-5p regulates the drug resistance of A549/DDP to cisplatin by targeting P-gp

Shen¹,

Xu²,

Yin³

2020

gpb

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In this study, we established the DDP-resistant NSCLC cell line A549/DDP to detect the effect of NORAD on cisplatin resistance of A549/DDP cells. NORAD was highly expressed in A549/DDP cells compared with A549 cells. The MTT data showed that knockdown of NORAD enhanced the inhibition rate of cisplatin on the A549/DDP cells and decreased IC50 value. The colony formation and MTT assay suggested that cisplatin inhibited cell proliferation, and knockdown of NORAD enhanced the inhibitory effect of cisplatin on A549/DDP cells. Besides, we found that NORAD silence reduced the P-gp expression but not BCRP, LRP and MRP. Moreover, NORAD could directly bind to miR-202-5p, and ABCB1 was a target of miR-202-5p. The MTT assay found that miR-202-5p inhibitor reversed the effects of NORAD silence on cisplatin resistance of A549/DDP cells. Then, the Western blot data showed that knockdown of NORAD reduced P-gp expression, and miR-202-5p inhibitor enhanced P-gp expression. ABCB1 overexpression reversed the inhibitory effect of NORAD knockdown on A549/DDP cells. Moreover, NORAD could directly bind to miR-202-5p, and ABCB1 was a target of miR-202-5p. Inhibition of miR-202-5p and overexpression of ABCB1 eliminated the effects of NORAD silence on cisplatin resistance of A549/DDP cells. Overexpression of miR-202-5p suppressed P-gp expression in A549/DDP cells. Collectively, our data showed that NORAD could enhance the DDP resistance of A549/DDP cells and potentially increased P-gp expression by sponging the miR-202-5p.

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Long non-coding RNA NORAD induces cell proliferation and migration in prostate cancer

Cited by 17 publications

References 21 publications

Long non-coding RNA NORAD exhaustion represses prostate cancer progression through inhibiting TRIP13 expression via competitively binding to miR-495-3p

Long non-coding RNA NORAD exhaustion represses prostate cancer progression through inhibiting TRIP13 expression via competitively binding to miR-495-3p

Silencing of Long Non-Coding RNA (LncRNA) Non-Coding RNA Activated by DNA Damage (NORAD) Inhibits Proliferation, Invasion, Migration, and Promotes Apoptosis of Glioma Cells via Downregulating the Expression of AKR1B1

LncRNA NORAD/miR-202-5p regulates the drug resistance of A549/DDP to cisplatin by targeting P-gp

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