Evidence map›Paper›PMID 30150766›Full record

ArticleNature communications2018

Group I Paks are essential for epithelial- mesenchymal transition in an Apc-driven model of colorectal cancer.

H Y Chow, B Dong, C A Valencia, C T Zeng, J N Koch, T Y Prudnikova, J Chernoff

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.4field-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

19 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Group I PAKs in myelin formation and repair of the central nervous system: what, when, and how.Biological reviews of the Cambridge Philosophical Society · 2022
    Review
  9. Article
  10. Article
  11. Article
  12. p21-Activated Kinase 1 Promotes Breast TumorigenesisFrontiers in cell and developmental biology · 2021
    Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. 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 3 institutions in 2 countries.

H Y ChowCancer Center, National Clinical Research Center for Geriatrics, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University and Collaborative Innovation Center for Biotherapy, 610041, Chengdu, Sichuan, China.
B DongCancer Center, National Clinical Research Center for Geriatrics, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University and Collaborative Innovation Center for Biotherapy, 610041, Chengdu, Sichuan, China.
C A ValenciaDivision of Human Genetics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, 45229, USA.
C T ZengCancer Center, National Clinical Research Center for Geriatrics, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University and Collaborative Innovation Center for Biotherapy, 610041, Chengdu, Sichuan, China.
J N KochCancer Biology Program, Fox Chase Cancer Center, Philadelphia, PA, 19111, USA.
T Y PrudnikovaCancer Biology Program, Fox Chase Cancer Center, Philadelphia, PA, 19111, USA.
J ChernoffCancer Biology Program, Fox Chase Cancer Center, Philadelphia, PA, 19111, USA. Jonathan.Chernoff@fccc.edu.ORCID http://orcid.org/0000-0002-4803-7836
Fox Chase Cancer Center · USSichuan University · CNCincinnati Children's Hospital Medical Center · US

Funding

WORD PROCESSING CENTER--COREP30CA006927 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI Eric Andrew Ross · 1985 to 2026
$138.8M
The Role of p21-Activated Kinases in Malignant MesotheliomaR01CA148805 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI CHERNOFF, JONATHAN, TESTA, JOSEPH R. · 2011 to 2020
$4.0M
Targeting the Kinome in Neurofibromatosis type 1R01CA142928 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI CHERNOFF, JONATHAN · 2010 to 2019
$3.9M
Targeting the Rac1 signaling pathway in malignant melanomaR01CA227184 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI CHERNOFF, JONATHAN · 2018 to 2022
$2.5M
NCI NIH HHS P30 CA006927NCI NIH HHS R01 CA142928NCI NIH HHS R01 CA148805NCI NIH HHS R01 CA227184
6 · The paper itself

Abstract

p21-activated kinases (Paks) play an important role in oncogenic signaling pathways and have been considered as potential therapeutic targets in various cancers. Most studies of Pak function employ gene knock-out or knock-down methods, but these approaches result in loss of both enzymatic and scaffolding properties of these proteins, and thus may not reflect the effects of small molecule inhibitors. Here we use a transgenic mouse model in which a specific peptide inhibitor of Group I Paks is conditionally expressed in response to Cre recombinase. Using this model, we show that inhibition of endogenous Paks impedes the transition of adenoma to carcinoma in an Apc-driven mouse model of colorectal cancer. These effects are mediated by inhibition of Wnt signaling through reduced β-catenin activity as well as suppression of an epithelial-mesenchymal transition program mediated by miR-200 and Snai1. These results highlight the potential therapeutic role of Pak1 inhibitors in colorectal cancer.

Indexed as

Adenomatous Polyposis ColiAnimalsApoptosisCell ProliferationColorectal NeoplasmsEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansMicep21-Activated KinasesProto-Oncogene Proteins p21(ras)Tumor Cells, CulturedWnt Signaling Pathwayp21-Activated KinasesProto-Oncogene Proteins p21(ras)

Identifiers

PMID30150766
PMCPMC6110733
OpenAlexW2888327045

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.