Evidence map›Paper›PMID 26618703›Full record

ArticlePloS one2015

Ribosomal L22-like1 (RPL22L1) Promotes Ovarian Cancer Metastasis by Inducing Epithelial-to-Mesenchymal Transition.

Nan Wu, Jia Wei, Yuhui Wang, Jinyan Yan, Ying Qin, Dandan Tong, Bo Pang, Donglin Sun, Haiming Sun, Yang Yu and 9 more

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in PloS one, 2015. 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 It has been retracted, and should not be counted.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 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

29 citing papers in PubMed, 52 citations in OpenAlex.

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  6. Intricate ribosome composition and translational reprogramming in epithelial-mesenchymal transition.Proceedings of the National Academy of Sciences of the United States of America · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors at 2 institutions in 2 countries.

Nan WuLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Jia WeiLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Yuhui WangLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Jinyan YanLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Ying QinLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Dandan TongDepartment of Pathology, Harbin Medical University, Harbin, China.
Bo PangLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Donglin SunLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Haiming SunLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Yang YuLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Wenjing SunLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Xiangning MengLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Chunyu ZhangLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Jing BaiLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Feng ChenLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Jingshu GengDepartment of Pathology, Third Affiliated Clinical Hospital, Harbin Medical University, Harbin, China.
Ki-Young LeeDepartment of Cell Biology & Anatomy, University of Calgary, Alberta, Canada.
Songbin FuLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Yan JinLaboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Harbin Medical University · CNUniversity of Calgary · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Double minute chromosomes (DMs) have important implications for cancer progression because oncogenes frequently amplified on them. We previously detected a functionally undefined gene amplified on DMs, Ribosomal L22-like1 (RPL22L1). The relationship between RPL22L1 and cancer progression is unknown. Here, RPL22L1 was characterized for its role in ovarian cancer (OC) metastasis and its underlying mechanism was examined. DNA copy number and mRNA expression of RPL22L1 in OC cells was analyzed using data obtained from The Cancer Genome Atlas and the Gene Expression Omnibus database. An immunohistochemical analysis of clinical OC specimens was performed and the relationships between expression level and clinicopathological factors were evaluated. Additionally, in vivo and in vitro assays were performed to understand the role of RPL22L1 in OC. RPL22L1 expression was higher in OC specimens than in normal tissues, and its expression level was highly positively correlated with invasion and lymph node metastasis (P < 0.05). RPL22L1 over-expression significantly enhanced intraperitoneal xenograft tumor development in nude mice and promoted invasion and migration in vitro. Additionally, RPL22L1 knockdown remarkably inhibited UACC-1598 cells invasion and migration. Further, RPL22L1 over-expression up-regulated the mesenchymal markers vimentin, fibronectin, and α-SMA, reduced expression of the epithelial markers E-cadherin, α-catenin, and β-catenin. RPL22L1 inhibition reduced expression of vimentin and N-cadherin. These results suggest that RPL22L1 induces epithelial-to-mesenchymal transition (EMT). Our data showed that the DMs amplified gene RPL22L1 is critical in maintaining the aggressive phenotype of OC and in triggering cell metastasis by inducing EMT. It could be employed as a novel prognostic marker and/or effective therapeutic target for OC.

Indexed as

Epithelial-Mesenchymal TransitionActinsAdultAnimalsbeta CateninBiomarkers, TumorCell Line, TumorFemaleFibronectinsHumansLymphatic MetastasisMiceMice, Inbred BALB CMice, NudeMiddle AgedOvarian NeoplasmsActinsbeta CateninBiomarkers, TumorFibronectinsRibosomal ProteinsRPL22L1 protein, humanRPL22L1 protein, mouseVimentin

Identifiers

PMID26618703
PMCPMC4664398
OpenAlexW2187240748

What OpenQuestion holds

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LicenceCC BY
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.