Evidence map›Paper›PMID 31653698›Full record

ArticleThe Journal of biological chemistry2019

Protein tyrosine phosphatase receptor type R (PTPRR) antagonizes the Wnt signaling pathway in ovarian cancer by dephosphorylating and inactivating β-catenin.

Yuetong Wang, Jian Cao, Weiwei Liu, Jiali Zhang, Zuo Wang, Yiqun Zhang, Linjun Hou, Shengmiao Chen, Piliang Hao, Liye Zhang and 4 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

17 citing papers in PubMed, 21 citations in OpenAlex.

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  8. [Risk modeling based on HER-2 related genes for bladder cancer survival prognosis assessment].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2023
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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

14 authors at 3 institutions in 1 country.

Yuetong WangSchool of Life Science and Technology, ShanghaiTech University, Shanghai 201210, China.
Jian CaoDepartment of Gynecology, Women's Hospital of Nanjing Medical University, Nanjing Maternity and Child Health Care Hospital, Nanjing 210004, China.
Weiwei LiuInstitute of Biophysics, Key Laboratory of RNA Biology, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Beijing 100101, China.
Jiali ZhangSchool of Life Science and Technology, ShanghaiTech University, Shanghai 201210, China.
Zuo WangSchool of Life Science and Technology, ShanghaiTech University, Shanghai 201210, China.
Yiqun ZhangInstitute of Biophysics, Key Laboratory of RNA Biology, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Beijing 100101, China.
Linjun HouSchool of Life Science and Technology, ShanghaiTech University, Shanghai 201210, China.
Shengmiao ChenSchool of Life Science and Technology, ShanghaiTech University, Shanghai 201210, China.
Piliang HaoSchool of Life Science and Technology, ShanghaiTech University, Shanghai 201210, China.
Liye ZhangSchool of Life Science and Technology, ShanghaiTech University, Shanghai 201210, China.
Min ZhuangSchool of Life Science and Technology, ShanghaiTech University, Shanghai 201210, China.
Yang YuInstitute of Biophysics, Key Laboratory of RNA Biology, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Beijing 100101, China.
Dake LiDepartment of Gynecology, Women's Hospital of Nanjing Medical University, Nanjing Maternity and Child Health Care Hospital, Nanjing 210004, China. Electronic address: lidake2002@163.com.
Gaofeng FanSchool of Life Science and Technology, ShanghaiTech University, Shanghai 201210, China. Electronic address: fangf@shanghaitech.edu.cn.
ShanghaiTech University · CNInstitute of Biophysics · CNNanjing Maternity and Child Health Care Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite a lack of mutations, accumulating evidence supports an important role for the Wnt/β-catenin pathway in ovarian tumorigenesis. However, the molecular mechanism that contributes to the aberrant activation of the Wnt signaling cascade in ovarian cancer has not been fully elucidated. Here, we found that protein tyrosine phosphatase receptor type R (PTPRR) suppressed the activation of the Wnt/β-catenin pathway in ovarian cancer. We performed an shRNA-based biochemical screen, which identified PTPRR as being responsible for tyrosine dephosphorylation of β-catenin on Tyr-142, a key site controlling the transcriptional activity of β-catenin. Of note, PTPRR was down-regulated in ovarian cancers, and ectopic PTPRR re-expression delayed ovarian cancer cell growth both

Indexed as

Animalsbeta CateninCell LineCell Line, TumorFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHEK293 CellsHumansMice, NudeOvarian NeoplasmsPhosphorylationReceptor-Like Protein Tyrosine Phosphatases, Class 7RNA InterferenceRNAi TherapeuticsSurvival Analysisbeta CateninReceptor-Like Protein Tyrosine Phosphatases, Class 7beta-cateninepigeneticsgene regulationovarian cancerphosphataseprotein tyrosine phosphatase receptor type R (PTPRR)signal transductiontumor suppressor genetyrosine phosphorylationWnt signaling

Identifiers

PMID31653698
PMCPMC6885612
OpenAlexW2981738740

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.