Evidence map›Paper›PMID 29512779›Full record

ArticleOncology reports2018

Suppression of YAP by DDP disrupts colon tumor progression.

Kun Li, Jiwei Guo, Yan Wu, Dan Jin, Hong Jiang, Chengxia Liu, Chengyong Qin

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in Oncology reports, 2018. 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 It has been retracted, and should not be counted.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 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. Context-dependent roles of YAP/TAZ in stem cell fates and cancer.Cellular and molecular life sciences : CMLS · 2021
    Review
  4. Article
  5. Vimentin as a target for the treatment of COVID-19.BMJ open respiratory research · 2020
    Article
  6. Article
  7. mMolecular cancer · 2020
    Article
  8. Article
  9. The Ambivalent Function of YAP in Apoptosis and Cancer.International journal of molecular sciences · 2018
    Review
  10. Article
  11. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 1 country.

Kun LiDepartment of Gastroenterology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, P.R. China.
Jiwei GuoCancer Research Institute, Binzhou Medical University Hospital, Binzhou, Shandong 256603, P.R. China.
Yan WuCancer Research Institute, Binzhou Medical University Hospital, Binzhou, Shandong 256603, P.R. China.
Dan JinDepartment of Pain Management, Binzhou Medical University Hospital, Binzhou, Shandong 256603, P.R. China.
Hong JiangDepartment of Anorectal Surgery, Binzhou Medical University Hospital, Binzhou, Shandong 256603, P.R. China.
Chengxia LiuDepartment of Gastroenterology, Binzhou Medical University Hospital, Binzhou, Shandong 256603, P.R. China.
Chengyong QinDepartment of Gastroenterology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, P.R. China.
Binzhou Medical University · CNBinzhou University · CNShandong Provincial Hospital · CNShandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colon cancer is a commonly diagnosed cancer that often has a poor prognosis. Combined with the development of drug resistance to cancer treatment agents the treatment efficacy of colon cancer can be limited. Activation of the oncogene YAP has been shown to be related to colon cancer progression and is associated with poor prognosis, drug resistance and metastasis, even under treatment. Cisplatin (DDP) is a commonly used drug that can control carcinoma progression, although its mechanisms are poorly understood. In the present study, we examined whether DDP specifically suppressed YAP in order to inhibit colon carcinoma progression. Our data revealed that Mst/Yap signaling was unusually activated in colon cancers, promoting cell proliferation and invasion. DDP treatment decreased the expression of YAP at both the transcriptional and post-translational levels, leading to cell cycle arrest, apoptosis and senescence in cancer cells, in addition to decreasing epithelial-to-mesenchymal transition, cell motility and in vitro cell invasion and migration. Ultimately, DDP increased the expression of E-cadherin and decreased the expression of vimentin. The present study also revealed that post-translational regulation of YAP phosphorylation controlled the subcellular distribution between the nucleus and the cytoplasm. In conclusion, the findings of the present study revealed that DDP was a suitable therapeutic candidate for colon cancer that specifically targets the Mst/Yap signaling pathway.

Indexed as

Down-RegulationAdaptor Proteins, Signal TransducingAdultAgedAged, 80 and overAnimalsCell CycleCell Line, TumorCell MovementCell ProliferationCell SurvivalCisplatinColonic NeoplasmsEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticAdaptor Proteins, Signal TransducingCisplatinPhosphoproteinsTranscription FactorsYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID29512779
PMCPMC5928767
OpenAlexW2792182189

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.