Evidence map›Paper›PMID 28692056›Full record

ArticleOncogene2017

PDZK1 inhibits the development and progression of renal cell carcinoma by suppression of SHP-1 phosphorylation.

T Tao, X Yang, J Zheng, D Feng, Q Qin, X Shi, Q Wang, C Zhao, Z Peng, H Liu and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
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

22 citing papers in PubMed.

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  13. PDZK1 induces resistance to apoptosis in esophageal adenocarcinoma cells.Esophagus : official journal of the Japan Esophageal Society · 2021
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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

12 authors.

T TaoDepartment of Biochemistry and Molecular Biology, Capital Medical University, Beijing, PR China.
X YangDepartment of Biochemistry and Molecular Biology, Capital Medical University, Beijing, PR China.
J ZhengDepartment of Biochemistry and Molecular Biology, Capital Medical University, Beijing, PR China.
D FengDepartment of Interventional Radiology, First Hospital of Shanxi Medical University, Taiyuan, PR China.
Q QinDepartment of Biochemistry and Molecular Biology, Capital Medical University, Beijing, PR China.
X ShiDepartment of Biochemistry and Molecular Biology, Capital Medical University, Beijing, PR China.
Q WangDepartment of Biochemistry and Molecular Biology, Capital Medical University, Beijing, PR China.
C ZhaoDepartment of Biochemistry and Molecular Biology, Capital Medical University, Beijing, PR China.
Z PengDepartment of Biochemistry and Molecular Biology, Capital Medical University, Beijing, PR China.
H LiuDepartment of Biochemistry and Molecular Biology, Capital Medical University, Beijing, PR China.
W G JiangCardiff China Medical Research Collaborative, Cardiff University School of Medicine, Heath Park, Cardiff, UK.
J HeDepartment of Biochemistry and Molecular Biology, Capital Medical University, Beijing, PR China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal cell carcinoma (RCC) is one of the most aggressive urologic cancers, however, the mechanism on supporting RCC carcinogenesis is still not clear. By using gene expression profile analysis and functional clustering, PDZ domain-containing 1 (PDZK1) was revealed to be downregulated in human clear cell renal cell carcinoma (ccRCC) samples, which was also verified in several independent public ccRCC data sets. Using PDZK1 overexpression and knockdown models in ccRCC cell lines, we demonstrated that PDZK1 inhibited cell proliferation, cell cycle G1/S phase transition, cell migration and invasion, indicating a tumor-suppressor role in the development and progression of ccRCC. Our study further demonstrated that PDZK1 inhibited cell proliferation and migration of ccRCC via targeting SHP-1. PDZK1 was further identified to suppress cell proliferation by blocking SHP-1 phosphorylation at Tyr536 via inhibition of the association between SHP-1 and PLCβ3, and then retarding Akt phosphorylation and promoting STAT5 phosphorylation in ccRCC cells. Moreover, the inhibitive effects of PDZK1 on SHP-1 phosphorylation and the tumor growth were verified in vivo by xenograft tumor studies. Accordingly, PDZK1 expression was negatively correlated with SHP-1 activation and phosphorylation, advanced pathologic stage, tumor weight and size, and prognosis of ccRCC patients. These findings have provided first lines of evidences that PDZK1 expression is negatively correlated with SHP-1 activation and poor clinical outcomes in ccRCC. PDZK1 was identified as a novel tumor suppressor in ccRCC by negating SHP-1 activity.

Indexed as

AnimalsApoptosisCarcinogenesisCarcinoma, Renal CellCarrier ProteinsCell Line, TumorCell MovementCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansMaleMembrane ProteinsMiceOncogene Protein v-aktCarrier ProteinsMembrane ProteinsOncogene Protein v-aktPDZK1 protein, humanPhospholipase C betaPLCB3 protein, humanProtein Tyrosine Phosphatase, Non-Receptor Type 6PTPN6 protein, human

Identifiers

PMID28692056

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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.