Evidence map›Paper›PMID 25919292›Full record

ArticlePloS one2015

Enhanced IMP3 Expression Activates NF-кB Pathway and Promotes Renal Cell Carcinoma Progression.

Xuelian Pei, Muhan Li, Jun Zhan, Yu Yu, Xiaofan Wei, Lizhao Guan, Hakan Aydin, Paul Elson, Ming Zhou, Huiying He and 1 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 It has been retracted, and should not be counted.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 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 15% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Pooled it
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  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 2 countries.

Xuelian PeiKey Laboratory of Carcinogenesis and Translational Research, Ministry of Education, and State Key Laboratory of Natural and Biomimetic Drugs, Peking University Health Science Center, Beijing, PR China; Department of Anatomy, Histology and Embryology, Peking University Health Science Center, Beijing, PR China; Department of Histology and Embryology and Key Laboratory of Xinjiang Endemic and Ethnic Diseases, Ministry of Education, Shihezi University School of Medicine, Shihezi, Xinjiang, PR China.
Muhan LiKey Laboratory of Carcinogenesis and Translational Research, Ministry of Education, and State Key Laboratory of Natural and Biomimetic Drugs, Peking University Health Science Center, Beijing, PR China; Department of Pathology, Peking University Health Science Center, Beijing, PR China.
Jun ZhanKey Laboratory of Carcinogenesis and Translational Research, Ministry of Education, and State Key Laboratory of Natural and Biomimetic Drugs, Peking University Health Science Center, Beijing, PR China; Department of Anatomy, Histology and Embryology, Peking University Health Science Center, Beijing, PR China.
Yu YuKey Laboratory of Carcinogenesis and Translational Research, Ministry of Education, and State Key Laboratory of Natural and Biomimetic Drugs, Peking University Health Science Center, Beijing, PR China; Department of Anatomy, Histology and Embryology, Peking University Health Science Center, Beijing, PR China.
Xiaofan WeiKey Laboratory of Carcinogenesis and Translational Research, Ministry of Education, and State Key Laboratory of Natural and Biomimetic Drugs, Peking University Health Science Center, Beijing, PR China; Department of Anatomy, Histology and Embryology, Peking University Health Science Center, Beijing, PR China.
Lizhao GuanKey Laboratory of Carcinogenesis and Translational Research, Ministry of Education, and State Key Laboratory of Natural and Biomimetic Drugs, Peking University Health Science Center, Beijing, PR China; Department of Anatomy, Histology and Embryology, Peking University Health Science Center, Beijing, PR China.
Hakan AydinInstitute of Pathology and Laboratory Medicine, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, Ohio, United States of America.
Paul ElsonDepartment of Quantitative Health Sciences, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, Ohio, United States of America.
Ming ZhouInstitute of Pathology and Laboratory Medicine, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, Ohio, United States of America.
Huiying HeKey Laboratory of Carcinogenesis and Translational Research, Ministry of Education, and State Key Laboratory of Natural and Biomimetic Drugs, Peking University Health Science Center, Beijing, PR China; Department of Pathology, Peking University Health Science Center, Beijing, PR China.
Hongquan ZhangKey Laboratory of Carcinogenesis and Translational Research, Ministry of Education, and State Key Laboratory of Natural and Biomimetic Drugs, Peking University Health Science Center, Beijing, PR China; Department of Anatomy, Histology and Embryology, Peking University Health Science Center, Beijing, PR China.
Peking University · CNCleveland Clinic · USState Key Laboratory of Natural and Biomimetic Drugs

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInsulin-like growth factor 2 mRNA binding protein 3 (IMP3) is expressed in metastatic and a subset of primary renal cell carcinoma (RCC). However, the role of IMP3 in RCC progression was poorly understood. We aim to uncover the mechanism of IMP3 in regulating clear cell RCC (CCRCC) progression and validate the prognostic significance of IMP3 in localized CCRCC.

methodsCaki-1 cells stably overexpressing IMP3 and Achn cells with knockdown of IMP3 were analyzed for cell migration and invasion by Transwell assay. RNA-seq was used to profile gene expression in IMP3-expressing Caki-1 cells. A cohort of 469 localized CCRCC patients were examined for IMP3 expression by immunohistochemistry using tumor tissue array.

resultsIMP3 promoted Caki-1 cell migration and invasion, whereas knockdown of IMP3 by RNAi inhibited Achn cell migration and invasion. Enhanced IMP3 expression activated NF-кB pathway and through which, it functioned in promoting the RCC cell migration. IMP3 expression in localized CCRCC was found to be associated with higher nuclear grade, higher T stage, necrosis and sarcomatoid differentiation (p< 0.001). Enhanced IMP3 expression was correlated with shorter recurrence-free and overall survivals. Multivariable analysis validated IMP3 as an independent prognostic factor for localized CCRCC patients.

conclusionIMP3 promotes RCC cell migration and invasion by activation of NF-кB pathway. IMP3 is validated to be an independent prognostic marker for localized CCRCC.

Indexed as

Disease ProgressionSignal TransductionAdultAgedAged, 80 and overBiomarkers, TumorCarcinoma, Renal CellCell Line, TumorCell MovementFemaleHumansKaplan-Meier EstimateKidney NeoplasmsMaleMiddle AgedMultivariate AnalysisBiomarkers, TumorIGF2BP3 protein, humanNF-kappa BRNA-Binding Proteins

Identifiers

PMID25919292
PMCPMC4412497
OpenAlexW2072391908

What Socratic holds

Textmetadata
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 Socratic graph.