Evidence map›Paper›PMID 30033448›Full record

ArticleBritish journal of cancer2018

Angiopoietin-like protein 3 blocks nuclear import of FAK and contributes to sorafenib response.

Yi Bao, Fu Yang, Bing Liu, Tangliang Zhao, Zhipeng Xu, Ying Xiong, Shuhan Sun, Le Qu, Linhui Wang

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.5field-weighted citation impact, top 16% 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

15 citing papers in PubMed, 29 citations in OpenAlex.

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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 3 institutions in 1 country.

Yi BaoDepartment of Urology, Changzheng Hospital, Second Military Medical University, Shanghai, 200003, China.
Fu YangDepartment of Medical Genetics, Second Military Medical University, Shanghai, 200433, China.
Bing LiuDepartment of Urology, Changzheng Hospital, Second Military Medical University, Shanghai, 200003, China.
Tangliang ZhaoDepartment of Urology, Changzheng Hospital, Second Military Medical University, Shanghai, 200003, China.
Zhipeng XuDepartment of Urology, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan, 250014, China.
Ying XiongDepartment of Urology, Changzheng Hospital, Second Military Medical University, Shanghai, 200003, China.
Shuhan SunDepartment of Medical Genetics, Second Military Medical University, Shanghai, 200433, China. shsun@vip.sina.com.
Le QuDepartment of Urology, Jinling Hospital, Nanjing University Clinical School of Medicine, Nanjing, 210002, China. septsoul@hotmail.com.
Linhui WangDepartment of Urology, Changzheng Hospital, Second Military Medical University, Shanghai, 200003, China. wanglinhui@smmu.edu.cn.
Second Military Medical University · CNNanjing University · CNShandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPoor drug response of sorafenib is a major challenge which reduces clinical benefit of renal cell carcinoma (RCC) patients. It is therefore of great clinical significance to elucidate the underlying mechanism to restore the therapeutic response to sorafenib.

methodsAngiopoietin-like protein 3 (ANGPTL3) protein levels were measured by western blot and immunohistochemistry in two cohorts of RCC patients. Loss-of-function and gain-of-function experiments were performed to investigate the biological roles of ANGPTL3 in response to sorafenib treatment in RCC cells. Human proteome microarray and immunoprecipitation analysis were performed to explore the molecular mechanisms underlying the functions of ANGPTL3.

resultsANGPTL3 was upregulated in sorafenib-responsive RCC, which correlated with clinically good sorafenib response. Knockdown of ANGPTL3 conferred sorafenib-tolerance traits to RCC cells, whereas overexpression of ANGPTL3 restored sorafenib sensitivity in RCC cells. Mechanistically, ANGPTL3 bound to Focal Adhesion Kinase(FAK) and restained sorafenib induced nuclear translocation of FAK, leading to attenuate the ubiquitination of p53, which contributed to cellular apoptosis and enhanced sorafenib response.

conclusionsANGPTL3 may be a novel predictor for the response of sorafenib therapy in RCC patients, and a potential target in improving its therapeutic effect.

Indexed as

Up-RegulationActive Transport, Cell NucleusAngiopoietin-Like Protein 3Angiopoietin-like ProteinsAnimalsCarcinoma, Renal CellCell Line, TumorCell NucleusFocal Adhesion Kinase 1Gene Expression Regulation, NeoplasticHumansKidney NeoplasmsMaleMiceSorafenibTreatment OutcomeAngiopoietin-Like Protein 3Angiopoietin-like ProteinsANGPTL3 protein, humanFocal Adhesion Kinase 1PTK2 protein, humanSorafenibTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID30033448
PMCPMC6134083
OpenAlexW2883345584

What OpenQuestion holds

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Registered trials

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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.