Evidence map›Paper›PMID 27121065›Full record

ArticleOncotarget2016

Wip1 suppresses ovarian cancer metastasis through the ATM/AKT/Snail mediated signaling.

Sheng Yin, Pan Wang, Lina Yang, Yang Liu, Yan Wang, Mingming Liu, Zihao Qi, Jiao Meng, Ting-Yan Shi, Gong Yang and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

  1. The role of PPM1D in cancer and advances in studies of its inhibitors.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2020
    Pooled it
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  7. Theasaponin EMolecules (Basel, Switzerland) · 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

11 authors at 3 institutions in 1 country.

Sheng YinDepartment of Gynecological Oncology, Fudan University Shanghai Cancer Center, Shanghai Medical College, Fudan University, Shanghai 200032, China.
Pan WangDepartment of Gynecological Oncology, Fudan University Shanghai Cancer Center, Shanghai Medical College, Fudan University, Shanghai 200032, China.
Lina YangDepartment of Gynecology and Obstetrics, The Fifth People's Hospital of Shanghai Fudan University, Shanghai 200240, China.
Yang LiuCancer Institute, Fudan University Shanghai Cancer Center, Shanghai Medical College, Fudan University, Shanghai 200032, China.
Yan WangCancer Institute, Fudan University Shanghai Cancer Center, Shanghai Medical College, Fudan University, Shanghai 200032, China.
Mingming LiuCancer Institute, Fudan University Shanghai Cancer Center, Shanghai Medical College, Fudan University, Shanghai 200032, China.
Zihao QiCancer Institute, Fudan University Shanghai Cancer Center, Shanghai Medical College, Fudan University, Shanghai 200032, China.
Jiao MengCancer Institute, Fudan University Shanghai Cancer Center, Shanghai Medical College, Fudan University, Shanghai 200032, China.
Ting-Yan ShiOvarian Cancer Program, Division of Gynecologic Oncology, Department of Gynecology and Obstetrics, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Gong YangCancer Institute, Fudan University Shanghai Cancer Center, Shanghai Medical College, Fudan University, Shanghai 200032, China.
Rongyu ZangOvarian Cancer Program, Division of Gynecologic Oncology, Department of Gynecology and Obstetrics, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Fudan University Shanghai Cancer Center · CNFudan University · CNZhongshan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inactivation of p53 greatly contributes to serous ovarian cancer, while the role of the wild-type p53 induced phosphatase 1 (Wip1) is quite unclear. In this study, by silencing or overexpression of Wip1, we found that Wip1 suppressed ovarian cancer cell invasion, migration, epithelial to mesenchymal transition (EMT), and ovarian cancer metastasis in xenograft animal models. Mechanistic studies showed that Wip1 may block ovarian cancer metastasis through inhibition of Snail and p-Akt expression because silencing or overexpression of Wip1 either upregulated or downregulated the expression of Snail and p-Akt (Ser 473), while further knockdown of Snail by shRNA or inhibition of p-Akt by a chemical compound attenuated cell invasion, migration and EMT in Wip1 silencing cells. We also found that the phosphorylation of Akt at Ser 473 might be mediated through p-ATM (Ser 1981). Thus, Wip1 may suppress ovarian cancer metastasis through negative regulation of p-ATM, p-Akt, and Snail, which was also evidenced in the limited clinical specimens. Therefore, our data may provide a novel therapeutic indication for serous ovarian cancer based on the uncovered mechanism associated with the precise function of Wip1 independent of p53.

Indexed as

AnimalsAtaxia Telangiectasia Mutated ProteinsCarcinoma, Ovarian EpithelialCell Line, TumorEpithelial-Mesenchymal TransitionFemaleHeterograftsHumansMiceNeoplasm InvasivenessNeoplasms, Glandular and EpithelialOvarian NeoplasmsProtein Phosphatase 2CProto-Oncogene Proteins c-aktSignal TransductionSnail Family Transcription FactorsAtaxia Telangiectasia Mutated ProteinsATM protein, humanPPM1D protein, humanProtein Phosphatase 2CProto-Oncogene Proteins c-aktSnail Family Transcription FactorsEMTmetastasisovarian cancerWip1

Identifiers

PMID27121065
PMCPMC5045401
OpenAlexW2341949310

What OpenQuestion 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 OpenQuestion graph.