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High expression of long non-coding RNA SBF2-AS1 promotes proliferation in non-small cell lung cancer

Overview of attention for article published in Journal of Experimental & Clinical Cancer Research, May 2016
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2 tweeters

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Title
High expression of long non-coding RNA SBF2-AS1 promotes proliferation in non-small cell lung cancer
Published in
Journal of Experimental & Clinical Cancer Research, May 2016
DOI 10.1186/s13046-016-0352-9
Pubmed ID
27154193
Authors

Junjie Lv, Mantang Qiu, Wenjia Xia, Chao Liu, Youtao Xu, Jie Wang, Xuechun Leng, Su Huang, Rong Zhu, Ming Zhao, Fengqing Ji, Lin Xu, Keping Xu, Rong Yin

Abstract

Recent evidence has proven that long noncoding RNAs (lncRNAs) play important roles in cancer biology, while few lncRNAs have been characterized in NSCLC. Here, we characterized a novel lncRNA, SBF2 antisense RNA 1 (SBF2-AS1), in non-small cell lung cancer (NSCLC). Quantitative real-time PCR was used to quantify SBF2-AS1 expression in NSCLC tissues and cell lines. The correlation of SBF2-AS1 expression with clinicopathologic features was analyzed in a cohort NSCLC patient. Loss of function and gain of function studies were performed to determine the effects of SBF2-AS1 on proliferation and metastasis of NSCLC cells. RNA immunoprecipitation and chromosome immunoprecipitation assay was performed to confirm the interaction between SBF2-AS1 with protein and chromosome. We confirmed that SBF2-AS1 was significantly upregulated in NSCLC compared with corresponding non-tumor tissues, and a high expression level of SBF2-AS1 was correlated with lymph node metastasis and advanced TNM stage. Using siRNAs specifically targeting SBF2-AS1 and plasmid vector, we successfully silenced and overexpressed SBF2-AS1 in NSCCLC cell lines and investigated its biological function both in vitro and in vivo. After the silencing of SBF2-AS1, the metastasis of NSCLC cells was significantly inhibited, the silencing of SBF2-AS1 decreased the proliferation of NSCLC cells, and the cell cycle was arrested at the G1 phase; while overexpression promoted proliferation ability. Xenograft tumor models revealed that the silencing of SBF2-AS1 inhibited tumor growth in vivo. We speculated that SBF2-AS1 might negatively regulate P21. RNA immunoprecipitation discovered that SBF2-AS2 could bind with a core component of polycomb repressive complex2, SUZ12. Additionally chromatin immunoprecipitation assay demonstrated that, after silencing SBF2-AS1, the enrichment of SUZ12 and trimethylation of histone 3 lysine 27 decreased at the promoter region of P21. We demonstrated that SBF2-AS1 is upregulated in NSCLC and promotes proliferation of NSCLC tumor cells. SBF2-AS1 may serve as a novel biomarker and potential therapeutic target for NSCLC patients.

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Twitter Demographics

The data shown below were collected from the profiles of 2 tweeters who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 63 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Sweden 1 2%
Unknown 62 98%

Demographic breakdown

Readers by professional status Count As %
Student > Postgraduate 24 38%
Student > Bachelor 12 19%
Student > Ph. D. Student 8 13%
Student > Doctoral Student 3 5%
Student > Master 3 5%
Other 5 8%
Unknown 8 13%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 32 51%
Agricultural and Biological Sciences 12 19%
Medicine and Dentistry 5 8%
Neuroscience 2 3%
Immunology and Microbiology 1 2%
Other 2 3%
Unknown 9 14%

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 08 May 2016.
All research outputs
#5,799,682
of 7,667,486 outputs
Outputs from Journal of Experimental & Clinical Cancer Research
#209
of 404 outputs
Outputs of similar age
#186,692
of 266,725 outputs
Outputs of similar age from Journal of Experimental & Clinical Cancer Research
#10
of 30 outputs
Altmetric has tracked 7,667,486 research outputs across all sources so far. This one is in the 13th percentile – i.e., 13% of other outputs scored the same or lower than it.
So far Altmetric has tracked 404 research outputs from this source. They receive a mean Attention Score of 1.5. This one is in the 29th percentile – i.e., 29% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 266,725 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 16th percentile – i.e., 16% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 30 others from the same source and published within six weeks on either side of this one. This one is in the 43rd percentile – i.e., 43% of its contemporaries scored the same or lower than it.

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