Long non‑coding RNA ZNF674‑1 acts as a cancer suppressor in nasopharyngeal carcinoma

Nie, Guohui; Zhao, Li; Duan, Hongfang; Luo, Liang; Hu, Hongyi; Chen, Xiaofan; Zhang, Wei

doi:10.3892/ol.2018.8540

Cited by 5 publications

(6 citation statements)

References 36 publications

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“…As miRNA sponges to play roles, lncRNAs are proven to regulate tumorigenesis [ 19 ]. We determined the localization of LINC00210 in NPC cells and found that it mainly located in the cytoplasm ( Figure 3 A), suggesting LINC00210 might be a miRNA sponge.…”

Section: Resultsmentioning

confidence: 99%

“…In NPC, a few of lncRNAs have been identified as indicators for patients’ prognosis. For instance, Nie et al [ 19 ] showed that lncRNA ZNF674-1 down-regulation predicts poor prognosis in NPC. Wu et al [ 25 ] showed that lncRNA ANRIL is up-regulated by SOX2 and promotes the growth of NPC cells.…”

Section: Discussionmentioning

confidence: 99%

“…Long RNAs are shown to sponge miRNAs in cancer [ 19 , 28 , 29 ]. We further investigated the target of LINC00210.…”

Section: Discussionmentioning

confidence: 99%

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LINC00210 as a miR-328-5p sponge promotes nasopharyngeal carcinoma tumorigenesis by activating NOTCH3 pathway

Zhang

Zhao

et al. 2018

Bioscience Reports

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As a kind of essential regulators, long noncoding RNAs (lncRNAs) have attracted a lot of attention in recent years. Nevertheless, the function of lncRNA in nasopharyngeal carcinoma (NPC) remains poorly understood. In the present study, we explained the role and mechanism of LINC00210 in NPC progression. We found that LINC00210 expression was up-regulated in NPC samples. Besides, its overexpression was positively correlated with NPC metastasis while predicting poor prognosis. Based on functional experiments, we revealed that LINC00210 contributed to NPC cell proliferation and invasion in vitro, and promotes tumor growth in vivo. Mechanistically, we identified that LINC00210 was located in the cytoplasm of NPC cells and served as the miR-328-5p sponge. Furthermore, we showed that miR-328-5p targets the 3′ untranslated region (3′-UTR) of NOTCH3. Through inhibiting miR-328-5p activity, LINC00210 promoted NOTCH3 expression in NPC, leading to activation of NOTCH3 signaling pathway. In conclusion, our study indicates LINC00210 promotes NPC progression through modulating proliferation and invasion.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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LINC00210 as a miR-328-5p sponge promotes nasopharyngeal carcinoma tumorigenesis by activating NOTCH3 pathway

Zhang

Zhao

et al. 2018

Bioscience Reports

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“…It is well known that long noncoding RNAs (lncRNAs) are generally longer than 200 nucleotides and have no ability to be translated into proteins. 5 Extensive investigations have proven that lncRNAs are implicated in a variety of cellular processes, such as cell proliferation, cell cycle, cell metastasis, and cell apoptosis. 6 LncRNA n326322 promotes the proliferation and invasion in NPC.…”

Section: Introductionmentioning

confidence: 99%

LncRNA SOX2‐OT regulates proliferation and metastasis of nasopharyngeal carcinoma cells through miR‐146b‐5p/HNRNPA2B1 pathway

Enqin¹,

2019

J of Cellular Biochemistry

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Nasopharyngeal carcinoma (NPC) is an aggressive malignancy with a high mortality on account of its frequent metastasis and poor prognosis. An extensive body of investigations has proven that long noncoding RNAs are implicated in a variety of biological processes. Although SOX2‐OT has been reported to play an oncogenic role in osteosarcoma, the mechanism of SOX2‐OT‐driven NPC progression is still obscure. The aim of this study was to elucidate the biological function of SOX2‐OT and the related possible mechanism in NPC. In our study, SOX2‐OT was notably elevated in NPC samples and cells. Further, a high expression level of SOX2‐OT was correlated with poor clinical outcomes of NPC. Results from loss‐of‐function experiments suggested that knockdown of SOX2‐OT repressed cell proliferation, arrested cell cycle, facilitated cell apoptosis, and inhibited cell metastasis of NPC. To further investigate the molecular mechanism of SOX2‐OT, miR‐146b‐5p was found to directly bind to SOX2‐OT, which mediated the role of SOX2‐OT in NPC tumorigenesis. In addition, HNRNPA2B1 was a target of miR‐146b‐5p and SOX2‐OT modulated the expression of HNRNPA2B1 through competitively binding to miR‐146b‐5p. At last, we discovered that SOX2‐OT regulated NPC progression by targeting miR‐146b‐5p/HNRNPA2B1 pathway, which may provide more innovative targets for the treatment of patients with NPC.

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“…A vast number of lncRNAs are aberrantly expressed in NPC. For instance, NEAT1,12 DANCR,13 and HOTTIP14 are overexpressed in NPC and function as oncogenes, whereas ZNF674-1,15 LET,16 and LINC008617 are underexpressed in NPC and exert tumor-suppressive actions. Therefore, lncRNAs may represent useful therapeutic targets in NPC.…”

Section: Introductionmentioning

confidence: 99%

<p>LINC00958 Promotes The Malignancy Of Nasopharyngeal Carcinoma By Sponging microRNA-625 And Thus Upregulating NUAK1</p>

Chen¹,

Xu²,

Zhang³

et al. 2019

OTT

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PurposeThe aberrant expression of long noncoding RNAs (lncRNAs) indicates progression of various diseases. LINC00958 has been well studied in several types of human cancer; however, the expression profile, functions, and potential mechanism of action of this lncRNA in nasopharyngeal carcinoma (NPC) remain largely unclear and still need to be elucidated. In the present study, we aimed to measure LINC00958 expression in NPC, determine its clinical value, and explore its roles in NPC progression as well as the mechanisms behind these processes.MethodsThe expression profile of LINC00958 in NPC was evaluated by reverse-transcription quantitative polymerase chain reaction (RT-qPCR). A series of functional assays, including the Cell Counting Kit-8 assay, flow cytometry, a Transwell assay, and an in vivo nude mouse model, were utilized to determine the participation of LINC00958 in the malignancy of NPC.ResultsLINC00958 was found to be upregulated in NPC tissue specimens and cell lines. The LINC00958 overexpression significantly correlated with tumor size, lymph node status, TNM stage, and worse overall survival among NPC patients. Downregulation of LINC00958 suppressed NPC cell proliferation, migration, and invasion and induced apoptosis in vitro. Additionally, the LINC00958 knockdown impaired tumor growth in vivo. Mechanistically, LINC00958 was found to serve as a molecular sponge of microRNA-625 (miR-625), thereby upregulating NUAK family SNF1-like kinase 1 (NUAK1) in NPC cells. Lastly, rescue experiments validated the involvement of the miR-625–NUAK1 axis in LINC00958-mediated biological functions in NPC.ConclusionOur results demonstrated that LINC00958 works as an oncogene in NPC and plays a key role in the malignant phenotype of NPC cells by sponging miR-625 and increasing NUAK1 expression. The LINC00958–miR-625–NUAK1 pathway might be a target for anticancer therapy in patients with NPC.

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Long non‑coding RNA ZNF674‑1 acts as a cancer suppressor in nasopharyngeal carcinoma

Cited by 5 publications

References 36 publications

LINC00210 as a miR-328-5p sponge promotes nasopharyngeal carcinoma tumorigenesis by activating NOTCH3 pathway

LINC00210 as a miR-328-5p sponge promotes nasopharyngeal carcinoma tumorigenesis by activating NOTCH3 pathway

LncRNA SOX2‐OT regulates proliferation and metastasis of nasopharyngeal carcinoma cells through miR‐146b‐5p/HNRNPA2B1 pathway

<p>LINC00958 Promotes The Malignancy Of Nasopharyngeal Carcinoma By Sponging microRNA-625 And Thus Upregulating NUAK1</p>

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