Evidence map›Paper›PMID 26446789›Full record

ArticleThe Journal of biological chemistry2015

Long Non-coding RNA Growth Arrest-specific Transcript 5 (GAS5) Inhibits Liver Fibrogenesis through a Mechanism of Competing Endogenous RNA.

Fujun Yu, Jianjian Zheng, Yuqing Mao, Peihong Dong, Zhongqiu Lu, Guojun Li, Chuanyong Guo, Zhanju Liu, Xiaoming Fan

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed, 2 pooled it
6.6field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

87 citing papers in PubMed, 2 syntheses or guidelines pooled it, 147 citations in OpenAlex.

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27 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 5 institutions in 1 country.

Fujun YuDepartment of Gastroenterology, Jinshan Hospital of Fudan University, Jinshan, Shanghai 201508, China.
Jianjian ZhengWenzhou Key Laboratory of Surgery.
Yuqing MaoDepartment of Gastroenterology, Jinshan Hospital of Fudan University, Jinshan, Shanghai 201508, China.
Peihong DongDepartments of Infectious Diseases.
Zhongqiu LuEmergency, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China.
Guojun LiDepartment of Hepatology, Ningbo Yinzhou Second Hospital, Ningbo 315000, China.
Chuanyong GuoDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, China.
Zhanju LiuDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, China.
Xiaoming FanDepartment of Gastroenterology, Jinshan Hospital of Fudan University, Jinshan, Shanghai 201508, China; Department of Internal Medicine, Shanghai Medical College, Fudan University, Shanghai 201508, China. Electronic address: ktsqdph@163.com.
Jinshan Hospital of Fudan University · CNFirst Affiliated Hospital of Wenzhou Medical University · CNNingbo No. 2 Hospital · CNShanghai Tenth People's Hospital · CNTongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Effective control of hepatic stellate cell (HSC) activation and proliferation is critical to the treatment of liver fibrosis. Long non-coding RNAs have been shown to play a pivotal role in the regulation of cellular processes. It has been reported that growth arrest-specific transcript 5 (GAS5) acts as a crucial mediator in the control of cell proliferation and growth. However, little is known about the role and underlying mechanism of GAS5 in liver fibrosis. In this study, our results indicated that GAS5 expression was reduced in mouse, rat, and human fibrotic liver samples and in activated HSCs. Overexpression of GAS5 suppressed the activation of primary HSCs in vitro and alleviated the accumulation of collagen in fibrotic liver tissues in vivo. We identified GAS5 as a target of microRNA-222 (miR-222) and showed that miR-222 could inhibit the expression of GAS5. Interestingly, GAS5 could also repress miR-222 expression. A pulldown assay further validated that GAS5 could directly bind to miR-222. As a competing endogenous RNAs, GAS5 had no effect on primary miR-222 expression. In addition, GAS5 was mainly localized in the cytoplasm. Quantitative RT-PCR further demonstrated that the copy numbers of GAS5 per cell are higher than those of miR-222. GAS5 increased the level of p27 protein by functioning as a competing endogenous RNA for miR-222, thereby inhibiting the activation and proliferation of HSCs. Taken together, a new regulatory circuitry in liver fibrosis has been identified in which RNAs cross-talk by competing for shared microRNAs. Our findings may provide a new therapeutic strategy for liver fibrosis.

Indexed as

AnimalsLiver CirrhosisMaleMiceMice, Inbred C57BLRNARNA, Long NoncodingGAS5 long non-coding RNA, humanRNARNA, Long Noncodingcompeting endogenous RNAfibrosisgrowth arrest-specific transcript 5hepatic stellate cell (HSC)liver fibrosislong non-coding RNA (long ncRNA, lncRNA)microRNA-222microRNA (miRNA)RNA interference (RNAi)

Identifiers

PMID26446789
PMCPMC4653684
OpenAlexW2276550096

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.