Genome‐wide analysis of long non‐coding <scp>RNA</scp> in primary nasopharyngeal carcinoma by microarray

Qiu, Yang; Deng, Yanfei

doi:10.1111/his.12616

Cited by 35 publications

(25 citation statements)

References 14 publications

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“…However, the roles and mechanisms of EWSAT1 in NPC have not been well elaborated. Yang and his colleagues have reported that EWSAT1 (LINC00277) is highly expressed in NPC (6.85-fold than NP tissues) [14]. Our present study added new evidence that over-expression of EWSAT1 owned oncogenic roles in NPC.…”

Section: Discussionsupporting

confidence: 66%

“…It has been reported that knockdown of EWSAT1 decreases soft agar colony growth of Ewing sarcoma cell lines [7], which indicated that EWSAT1 exerted an essential role on the occurrence, development and progression of malignant tumors. Recently, Yang and his colleagues has reported that EWSAT1 is highly expressed in NPC (6.85-fold than NP tissues) [14], while up to date, there is no related study elaborating the relevance between EWSAT1 expression and NPC progression. Hence, the role of EWSAT1 on NPC and its potential biological mechanisms still remain to be explored.…”

Section: Introductionmentioning

confidence: 99%

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Long non-coding RNA EWSAT1 promotes human nasopharyngeal carcinoma cell growth in vitro by targeting miR-326/-330-5p

Song

Yin

2016

Aging

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Long non-coding RNA (lncRNA) Ewing sarcoma associated transcript 1 (EWSAT1) has been identified as an oncogene, and its dysregulation is closed corrected with tumor progression in Ewing sarcoma. Recently, high-through put analysis reveals that EWSAT1 is also highly expressed in human nasopharyngeal carcinoma (NPC). However, whether the aberrant expression of EWSAT1 in NPC is corrected with malignancy or prognosis has not been expounded. Herein, we identified that EWSAT1 was up-regulated in NPC tissues and cell lines, and higher expression of EWSAT1 resulted in a markedly poorer survival time. EWSAT1 over-expression facilitated, while EWSAT1 silencing impaired cell growth in NPC. In addition, mechanistic analysis demonstrated that EWSAT1 up-regulated the expression of miR-326/330-5p clusters targeted gene cyclin D1 through acting as a competitive ‘sponge’ of miR-326/330-5p clusters. Collectively, our data revealed that EWSAT1 promotes NPC cell growth in vitro through up-regulating cyclin D1 partially via ‘spongeing’ miR-326/330-5p clusters.

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Section: Discussionsupporting

confidence: 66%

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA EWSAT1 promotes human nasopharyngeal carcinoma cell growth in vitro by targeting miR-326/-330-5p

Song

Yin

2016

Aging

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“…Bo et al [29] showed that AFAP1-AS1 promoted NPC cell metastasis via regulation of actin filament integrity. There are also several studies that have clarified the expression patterns of lncRNAs in NPC focusing on paired analyses of different types of tissues [30,31,32]. However, few studies have explored the relationships between dysregulated expression of lncRNAs and metastasis in NPC, especially using models based on cell lines.…”

Section: Discussionmentioning

confidence: 99%

Microarray Expression Profiling of Long Non-Coding RNAs Involved in Nasopharyngeal Carcinoma Metastasis

Wen

Tang

et al. 2016

IJMS

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Increasing evidence has demonstrated a significant role for long non-coding RNAs (lncRNAs) in tumorigenesis. However, their functions in nasopharyngeal carcinoma (NPC) metastasis remain largely unknown. In this study, a model comparing high and low metastatic NPC cell lines (5-8F vs. 6-10B and S18 vs. S26) was constructed to determine the expression profile of lncRNAs using the microarray analysis, and we found 167 lncRNAs and 209 mRNAs were differentially expressed. Bioinformatic analysis indicated that the dysregulated mRNAs participated in important biological regulatory functions in NPC. Validation of 26 significantly dysregulated lncRNAs by qRT-PCR showed the expression patterns of 22 lncRNAs were in accordance with the microarray data. Furthermore, the expression level of ENST00000470135, which was the most upregulated lncRNA in high metastatic cell lines, was significantly higher in NPC cell lines and tissues with lymph node metastasis (LNM) and knocking down ENST00000470135 suppressed the migration, invasion and proliferation of NPC cells in vitro. In conclusion, our study revealed expression patterns of lncRNAs in NPC metastasis. The dysregulated lncRNAs may act as novel biomarkers and therapeutic targets for NPC.

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“…They have been shown to be deregulated in many cancers and participate in carcinogenesis and cancer progression by modulating the expression of many oncogenes or tumor suppressor genes [14][15][16]. However, there are only several studies of lncRNAs in human NPC, and the expressions and functions of lncRNAs in NPC remain largely unknown [17][18][19][20]. LncRNA-LET, a recently identified lncRNA, has been reported to be downregulated and exhibit tumor-suppressive roles in hepatocellular carcinoma, cervical cancer, gastric cancer, and gallbladder cancer [21][22][23][24].…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA-LET, which is repressed by EZH2, inhibits cell proliferation and induces apoptosis of nasopharyngeal carcinoma cell

Sun

Liu

et al. 2015

Med Oncol

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Recent studies have reported that long noncoding RNAs (lncRNAs) play critical roles in carcinogenesis and progression. LncRNA-LET, a recently identified lncRNA, has been shown to be a tumor suppressor in hepatocellular carcinoma. However, the expression and functional of lncRNA-LET in other type of cancers remain largely unknown. In this study, we found that lncRNA-LET was significantly downregulated in nasopharyngeal carcinoma (NPC) tissues compared with corresponding normal tissues. Decreased LET expression is significantly correlated with advanced clinical stage, larger tumor size, increased lymph node tumor burden, and poor survival of NPC patients. Gain- and loss-of-function experiments demonstrated that enhanced LET expression inhibited NPC cells proliferation and induced cell apoptosis. By contrast, the knockdown of LET promoted NPC cells proliferation and inhibited cell apoptosis. Importantly, we found lncRNA-LET is transcriptional repressed by EZH2-mediated H3K27 histone methylation on the LET promoter. The expressions of EZH2 and lncRNA-LET are significantly inversely correlated in NPC tissues. Collectively, these findings indicate a pivotal role for lncRNA-LET in NPC cell proliferation and apoptosis, and reveal an epigenetic mechanism for lncRNA-LET dysregulation.

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Genome‐wide analysis of long non‐coding RNA in primary nasopharyngeal carcinoma by microarray

Abstract: This study could provide new insight into the molecular mechanisms of lncRNAs and their potential role in NPC for further study. These differentially expressed lncRNAs may act as novel biomarkers and therapeutic targets for NPC.

Cited by 35 publications

References 14 publications

Long non-coding RNA EWSAT1 promotes human nasopharyngeal carcinoma cell growth in vitro by targeting miR-326/-330-5p

Long non-coding RNA EWSAT1 promotes human nasopharyngeal carcinoma cell growth in vitro by targeting miR-326/-330-5p

Microarray Expression Profiling of Long Non-Coding RNAs Involved in Nasopharyngeal Carcinoma Metastasis

Long noncoding RNA-LET, which is repressed by EZH2, inhibits cell proliferation and induces apoptosis of nasopharyngeal carcinoma cell

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