Long non-coding RNA NEAT1 facilitates pancreatic cancer progression through negative modulation of miR-506-3p

Huang, Bo; Liu, Chuan; Wu, Qiong; Zhang, Jing; Min, Qing‐Hua; Sheng, Tianle; Wang, Xiaozhong; Zou, Yeqing

doi:10.1016/j.bbrc.2016.11.120

Cited by 73 publications

(69 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…36 miR-744 can inhibit GC cell proliferation and invasion through targeting neurotrophic factor. 18,19 LncRNA BC032469 can promote GC proliferation by upregulating hTERT and sponging miR-1207-5p. A, Binding region between miR-506 and NEAT1.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Long noncoding RNA NEAT1‐modulated miR‐506 regulates gastric cancer development through targeting STAT3

Tan

Wang

Liu

et al. 2019

J of Cellular Biochemistry

View full text Add to dashboard Cite

Accumulating evidence has indicated that lncRNA NEAT1 exerts critical roles in cancers. So far, the detailed biological role and mechanisms of NEAT1 which are responsible for human gastric cancer (GC) is still largely unknown. Here, we observed that NEAT1 and STAT3 expression were significantly upregulated in human gastric cancer cells including BGC823, SGC-7901, AGS, MGC803 and MKN28 cells compared to normal gastric epithelial cells GES-1 while miR-506 was downregulated. We inhibited NEAT1 and observed that NEAT1 inhibition was able to repress the growth, migration and invasion of gastric cancer cells. Reversely, overexpression of NEAT1 exhibited an increase ability of gastric cancer progression in BGC823 and SGC-7901 cells. Bioinformatics analysis, dual luciferase reporter assays, RIP assays and RNA pull-down tests validated the negative binding correlation between NEAT1 and miR-506. In addition, it was found that miR-506 can modulate expression of NEAT1 in vitro. STAT3 was predicted as an mRNA target of miR-506 and miR-506 mimics can suppress STAT3 mRNA expression. Subsequently, it was observed that downregulation of NEAT1 can restrain gastric cancer development by decreasing STAT3 which can be reversed by miR-506 inhibitors. Therefore, it was hypothesized in our study that NEAT1 can be recognized as a ceRNA to modulate STAT3 by sponging miR-506 in gastric cancer. In conclusion, we implied that NEAT1 can serve as an important biomarker in gastric cancer diagnosis and treatment. This article is protected by copyright. All rights reserved.

show abstract

Section: Discussionmentioning

confidence: 99%

“…14 Downregulation of miR-506 can promote pancreatic cancer development and chemoresistance through the SPHK1/Akt/NF-κB signaling. 18,19 Our study focused on the biological role of NEAT1 in GC. 16 Long noncoding RNA (lncRNA) MALAT1 can regulate miR-506 and modulate ovarian cancer through targeting iASPP.…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA NEAT1‐modulated miR‐506 regulates gastric cancer development through targeting STAT3

Tan

Wang

Liu

et al. 2019

J of Cellular Biochemistry

View full text Add to dashboard Cite

show abstract

“…miR-365 inhibition abrogated the inhibitory effect of NEAT1 knockdown. Several other miRNAs, including miR-377, miR-335, miR-107, miR-98 and miR-506, were identified to interact with NEAT1 in different types of cancers (12,14,(26)(27)(28), suggesting that NEAT1 plays an oncogenic role in different types of cancer through the regulation of different miRNAs.…”

Section: Discussionmentioning

confidence: 99%

lncRNA NEAT1 promotes cell proliferation and invasion by regulating miR‑365/RGS20 in oral squamous cell carcinoma

Huang

He²,

Wei

2018

Oncol Rep

View full text Add to dashboard Cite

Long non-coding RNAs (lncRNAs) have emerged as critical regulators of tumor progression. However, the function and mechanism of lncRNA NEAT1 in oral squamous cell carcinoma (OSCC) are unclear. In the present study, NEAT1 was significantly upregulated in OSCC cells and tissues. High expression of NEAT1 was correlated with advanced TNM stage and poor survival of patients. Using bioinformatics prediction and experimental analysis, we determined that NEAT1 could negatively regulate the expression of miR-365. The expression of miR-365 was decreased in OSCC tissues and inversely correlated with NEAT1 in tumors. Functionally, knockdown of NEAT1 significantly inhibited cell proliferation and invasion and induced cell cycle arrest at the G0/G1 phase and apoptosis, whereas inhibition of miR-365 abolished the suppressive effect of NEAT1 knockdown on cellular processes. RGS20, a direct target of miR-365, could reverse the tumor suppressive role of miR-365 mimic by enhancing cell viability and motility. Moreover, the protein levels of RGS20, cyclin D1, E-cadherin, N-cadherin and vimentin could be regulated by the NEAT1/miR-365 axis. NEAT1 silencing also inhibited tumor growth in vivo. Collectively, we revealed that the NEAT1/miR-365/RGS20 axis may be a novel mechanism or therapeutic strategy for OSCC treatment.

show abstract

“…For example, Zhang et al found that lncRNA ANRIL promoted CC carcinogenesis via PI3K/Akt pathways [8]. Zhang et al found that lncRNA PVT1 facilitated CC progression through negative modulation of miR-128-3p [9]. Guo et al revealed that lncRNA SNHG20 promoted CC cells proliferation and invasion via miR-140-5p-ADAM10 axis [10].…”

Section: Introductionmentioning

confidence: 99%

LncRNA SBF2-AS1 promotes the progression of cervical cancer by regulating miR-361-5p/FOXM1 axis

Gao

Feng

Yao

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

View full text Add to dashboard Cite

Long non-coding RNAs (lncRNAs) have been identified as critical players in tumorigenesis. Previous studies revealed that lncRNA SBF2-AS1 was involved in tumor progression. However, the role and underlying mechanism of SBF2-AS1 in cervical cancer (CC) remain unknown. In the present study, our data showed that SBF2-AS1 expression was significantly increased in CC. High SBF2-AS1 expression was associated with advanced FIGO stage and lymph node metastasis of CC patients. Function assays showed that SBF2-AS1 inhibition significantly reduced CC cells proliferation both in vitro and in vivo. Mechanistically, we showed that SBF2-AS1 upregulation restrained the activity of miR-361-5p and led to overexpression of FOXM1 in CC cells. Furthermore, we found that miR-361-5p inhibitors could rescue the effects of SBF2-AS1 inhibition on CC cells proliferation. Taken together, we demonstrated that the SBF2-AS1/miR-361-5p/FOXM1 axis might play an important role in CC progression. SBF2-AS1 might serve as a potential therapeutic target for CC treatment.

show abstract

Long non-coding RNA NEAT1 facilitates pancreatic cancer progression through negative modulation of miR-506-3p

Cited by 73 publications

References 23 publications

Long noncoding RNA NEAT1‐modulated miR‐506 regulates gastric cancer development through targeting STAT3

Long noncoding RNA NEAT1‐modulated miR‐506 regulates gastric cancer development through targeting STAT3

lncRNA NEAT1 promotes cell proliferation and invasion by regulating miR‑365/RGS20 in oral squamous cell carcinoma

LncRNA SBF2-AS1 promotes the progression of cervical cancer by regulating miR-361-5p/FOXM1 axis

Contact Info

Product

Resources

About