Evidence map›Paper›PMID 32585630›Full record

ArticleMolecular therapy. Nucleic acids2020

Long Noncoding RNA OIP5-AS1 Promotes the Progression of Liver Hepatocellular Carcinoma via Regulating the hsa-miR-26a-3p/EPHA2 Axis.

Yu-Shui Ma, Kai-Jian Chu, Chang-Chun Ling, Ting-Miao Wu, Xu-Chao Zhu, Ji-Bin Liu, Fei Yu, Zhi-Zhen Li, Jing-Han Wang, Qing-Xiang Gao and 9 more

RetractedOpen access · goldAbstract readRetracted Publication
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular therapy. Nucleic acids, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

16 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
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  3. The role of lncRNA OIP5-AS1 in cancer development and progression.Apoptosis : an international journal on programmed cell death · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors at 8 institutions in 1 country.

Yu-Shui MaShanghai Engineering Research Center of Molecular Therapeutics and New Drug Development, College of Chemistry and Molecular Engineering, East China Normal University, Shanghai 200062, China; Central Laboratory for Medical Research, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, China.
Kai-Jian ChuDepartment of Biliary Tract Surgery I, Eastern Hepatobiliary Surgery Hospital, Shanghai 200438, China.
Chang-Chun LingDepartment of General Surgery, The Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu Province, China.
Ting-Miao WuDepartment of Radiology, The Forth Affiliated Hospital of Anhui Medical University, Hefei 230012, China.
Xu-Chao ZhuCentral Laboratory for Medical Research, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, China.
Ji-Bin LiuCancer Institute, Nantong Tumor Hospital, Nantong 226631, China.
Fei YuCentral Laboratory for Medical Research, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, China.
Zhi-Zhen LiDepartment of Biliary Tract Surgery I, Eastern Hepatobiliary Surgery Hospital, Shanghai 200438, China.
Jing-Han WangDepartment of Biliary Tract Surgery I, Eastern Hepatobiliary Surgery Hospital, Shanghai 200438, China.
Qing-Xiang GaoDepartment of Biliary Tract Surgery I, Eastern Hepatobiliary Surgery Hospital, Shanghai 200438, China.
Bin YiDepartment of Biliary Tract Surgery I, Eastern Hepatobiliary Surgery Hospital, Shanghai 200438, China.
Hui-Min WangCentral Laboratory for Medical Research, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, China.
Li-Peng GuCentral Laboratory for Medical Research, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, China.
Liu LiCentral Laboratory for Medical Research, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, China.
Lin-Lin TianCentral Laboratory for Medical Research, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, China.
Yi ShiCentral Laboratory for Medical Research, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, China.
Xiao-Qing JiangDepartment of Biliary Tract Surgery I, Eastern Hepatobiliary Surgery Hospital, Shanghai 200438, China.
Da FuCentral Laboratory for Medical Research, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, China; Department of Radiology, The Forth Affiliated Hospital of Anhui Medical University, Hefei 230012, China. Electronic address: fu800da900@126.com.
Xiong-Wen ZhangShanghai Engineering Research Center of Molecular Therapeutics and New Drug Development, College of Chemistry and Molecular Engineering, East China Normal University, Shanghai 200062, China. Electronic address: xwzhang@sat.ecnu.edu.cn.
Second Military Medical University · CNShanghai Tenth People's Hospital · CNTongji University · CNEast China Normal University · CNEastern Hepatobiliary Surgery Hospital · CNAffiliated Hospital of Nantong University · CNAnhui Medical University · CNNantong Tumor Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Numerous studies have suggested that dysregulated long noncoding RNAs (lncRNAs) contributed to the development and progression of many cancers. lncRNA OIP5 antisense RNA 1 (OIP5-AS1) has been reported to be increased in several cancers. However, the roles of OIP5-AS1 in liver hepatocellular carcinoma (LIHC) remain to be investigated. In this study, we demonstrated that OIP5-AS1 was upregulated in LIHC tissue specimens and its overexpression was associated with the poor survival of patients with LIHC. Furthermore, loss-of function experiments indicated that OIP5-AS1 promoted cell proliferation and inhibited cell apoptosis both in vitro and in vivo. Moreover, binding sites between OIP5-AS1 and hsa-miR-26a-3p as well as between hsa-miR-26a-3p and EPHA2 were confirmed by luciferase assays. Finally, a rescue assay was performed to prove the effect of the OIP5-AS1/hsa-miR-26a-3p/EPHA2 axis on LIHC cell biological behaviors. Based on all of the above findings, our results suggested that OIP5-AS1 promoted LIHC cell proliferation and invasion via regulating the hsa-miR-26a-3p/EPHA2 axis.

Indexed as

EPHA2hsa-miR-26a-3pLIHCOIP5-AS1prognosis

Identifiers

PMID32585630
PMCPMC7321793
OpenAlexW3033435930

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.