Evidence map›Paper›PMID 28618450›Full record

ArticleCell proliferation2017

SAV1 represses the development of human colorectal cancer by regulating the Akt-mTOR pathway in a YAP-dependent manner.

Jianwu Jiang, Wei Chang, Yang Fu, Yongshun Gao, Chunlin Zhao, Xiefu Zhang, Shuijun Zhang

Open access · bronzeAbstract read
In one paragraph

Article in Cell proliferation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
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  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
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  12. Hippo-Yap/Taz signaling: Complex network interactions and impact in epithelial cell behavior.Wiley interdisciplinary reviews. Developmental biology · 2020
    Review
  13. Article
  14. Review
  15. RHPCG: a database of the Regulation of the Hippo Pathway in Cancer Genome.Database : the journal of biological databases and curation · 2019
    Article
  16. Review
  17. Review
  18. Article
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

7 authors at 1 institution in 1 country.

Jianwu JiangDepartment of Gastrointestinal Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Wei ChangDepartment of Intensive Care Unit, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
Yang FuDepartment of Gastrointestinal Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Yongshun GaoDepartment of Gastrointestinal Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Chunlin ZhaoDepartment of Gastrointestinal Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Xiefu ZhangDepartment of Gastrointestinal Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Shuijun ZhangDepartment of Henan Key Laboratory of Digestive Organ Transplantation, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.ORCID http://orcid.org/0000-0002-0599-3289
First Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesSAV1 is a human homologue of Salvador that contains two protein-protein interaction modules known as WW domains and acts as a scaffolding protein. SAV1 participates in the development of diverse types of cancer. We aimed to investigate the role of SAV1 in human colorectal cancer. MATERIALS AND

methodsHuman colorectal cancer samples were used to study the expression of SAV1 and YAP. Loss-of-function and gain-of-function strategies were used to study the effects of SAV1 on colorectal cancer cell growth. Rapamycin was used to treat cells and mice to investigate the effect of mTOR signalling.

resultsSAV1 represses the development of colorectal cancer by inhibiting the Akt-mTOR signalling in a YAP-dependent manner. The mRNA and protein levels of SAV1 are down-regulated in human colorectal cancer tissues compared with adjacent non-cancer tissues. SAV1 knockdown promotes the growth of colorectal cancer cells in vitro and in vivo, whereas SAV1 overexpression leads to opposing results. SAV1 represses the activation of the Akt-mTOR signalling, and rapamycin treatment blunts the effects of SAV1 on in vitro and in vivo growth of colorectal cancer cells. Finally, we show that SAV1 promotes the phosphorylation and inactivation of YAP, which contributes to the effect of SAV1 on Akt-mTOR signalling pathway.

conclusionsSAV1 is a repressor during the development of human colorectal cancer by inhibiting the YAP-Akt-mTOR signalling pathway.

Indexed as

AdultAgedAnimalsCell Cycle ProteinsColorectal NeoplasmsDown-RegulationFemaleHumansMaleMiceMice, Inbred BALB CMice, NudeMiddle AgedNuclear ProteinsPhosphorylationProto-Oncogene Proteins c-aktCell Cycle ProteinsMTOR protein, humanNuclear ProteinsProto-Oncogene Proteins c-aktRNA, MessengerRNA, Small InterferingSAV1 protein, humanSirolimusTOR Serine-Threonine KinasesTranscription FactorsYY1AP1 protein, human

Identifiers

PMID28618450
PMCPMC6529088
OpenAlexW2625817492

What OpenQuestion holds

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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.