<scp>NEAT</scp>1: A novel cancer‐related long non‐coding <scp>RNA</scp>

Yu, Xuezhong; Li, Zheng; Zheng, Heyi; Chan, Matthew T. V.; Wu, William Ka Kei

doi:10.1111/cpr.12329

Cited by 249 publications

(215 citation statements)

References 54 publications

(51 reference statements)

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“…Currently, there are no ideal biomarkers, which can be used in screening oesophageal cancer strategies . LncRNA nuclear paraspeckle assembly transcript 1 (NEAT1), LncRNA ANRIL, HOX transcript anti‐sense intergenic RNA (HOTAIR) and SOX2 overlapping transcript (SOX2OT) were found to be associated with oesophageal cancer …”

Section: Oesophageal Cancermentioning

confidence: 99%

Long non‐coding RNA PVT1: Emerging biomarker in digestive system cancer

Zhou

Liu

et al. 2017

Cell Proliferation

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The digestive system cancers are leading cause of cancer-related death worldwide, and have high risks of morbidity and mortality. More and more long non-coding RNAs (lncRNAs) have been studied to be abnormally expressed in cancers and play a key role in the process of digestive system tumour progression. Plasmacytoma variant translocation 1 (PVT1) seems fairly novel. Since 1984, PVT1 was identified to be an activator of MYC in mice. Its role in human tumour initiation and progression has long been a subject of interest. The expression of PVT1 is elevated in digestive system cancers and correlates with poor prognosis. In this review, we illustrate the various functions of PVT1 during the different stages in the complex process of digestive system tumours (including oesophageal cancer, gastric cancer, colorectal cancer, hepatocellular carcinoma and pancreatic cancer). The growing evidence shows the involvement of PVT1 in both proliferation and differentiation process in addition to its involvement in epithelial to mesenchymal transition (EMT). These findings lead us to conclude that PVT1 promotes proliferation, survival, invasion, metastasis and drug resistance in digestive system cancer cells. We will also discuss PVT1's potential in diagnosis and treatment target of digestive system cancer. There was a great probability PVT1 could be a novel biomarker in screening tumours, prognosis biomarkers and future targeted therapy to improve the survival rate in cancer patients.

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Section: Oesophageal Cancermentioning

confidence: 99%

Long non‐coding RNA PVT1: Emerging biomarker in digestive system cancer

Zhou

Liu

et al. 2017

Cell Proliferation

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“…The nuclear paraspeckle assembly transcript 1 (NEAT1) was a newly identified lncRNA that regulated gene expression by retaining mRNAs for editing in the nucleus (Clemson et al, ). It was reported as an oncogene in several types of human cancers, including hepatocellular carcinoma, lung cancer, oesophageal cancer, colorectal cancer, renal cell carcinoma, ovarian cancer, breast cancer, and glioma (F. Liu et al, ; Y. Liu, Wang, Fu, & Lu, ; Yu, Li, Zheng, Chan, & Wu, ; Zhou et al, ). However, the role of NEAT1 in RB remains unknown.…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA NEAT1 promotes the growth of human retinoblastoma cells via regulation of miR‐204/CXCR4 axis

Zhong

Yang

et al. 2018

Journal Cellular Physiology

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Retinoblastoma (RB) is an aggressive eye cancer of infancy and childhood with high mortality. Studies have shown that long noncoding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) is closely related to the progression of multiple cancers. However, its role in RB remains unknown. This study aimed to investigate the role and underlying mechanism of NEAT1 in RB. We first detected the expression of NEAT1 in human RB tissues and cell lines. The effects of NEAT1 on the proliferation, migration, and apoptosis of RB cells were analyzed by loss‐of‐function. The underlying mechanism of NEAT1 in RB was mainly focused on the microRNA 204/C‐X‐C chemokine receptor type 4 (miR‐204/CXCR4) axis. In addition, the role and mechanism of NEAT1 in RB were further evaluated in a mouse xenograft tumor model. We found NEAT1 and CXCR4 expression levels were elevated, whereas miR‐204 expression was decreased in RB tissues and cells. Downregulation of NEAT1 significantly decreased the proliferation and migration but promoted the apoptosis of RB cells. NEAT1 functioned as a competing endogenous RNA for miR‐204 to regulate CXCR4 expression. Knockdown of NEAT1 suppressed the tumor volume, tumor weight, and CXCR4 expression, whereas increased miR‐204 expression in mice. In conclusion, NEAT1 promotes the development of RB via miR‐204/CXCR4 axis, which provides a new target for the treatment of RB disease.

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“…[7][8][9][10][11][12] However, mutation of lncRNAs will cause cancer initiation and promote the metastasis of malignancy. [13][14][15] For instance, lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) was first found in lung cancer metastasis. Many studies had demonstrated that lncRNA MALAT1 was overexpressed in various cancer, and it might act as a potential biomarker and therapeutic target in cancer treatment.…”

Section: Introductionmentioning

confidence: 99%