Evidence map›Paper›PMID 31186061›Full record

ReviewJournal of experimental & clinical cancer research : CR2019

The roles of nuclear focal adhesion kinase (FAK) on Cancer: a focused review.

Jin Zhou, Qian Yi, Liling Tang

Open access · goldAbstract readReview
In one paragraph

Review in Journal of experimental & clinical cancer research : CR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 159 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
159citing papers in PubMed, 3 pooled it
21.4field-weighted citation impact, top 1% 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

159 citing papers in PubMed, 3 syntheses or guidelines pooled it, 298 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
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  10. Article
  11. Endometriosis and the Hallmarks of Cancer.Reproductive sciences (Thousand Oaks, Calif.) · 2026
    Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Activation of Focal Adhesion Pathway byAnimals : an open access journal from MDPI · 2025
    Article
  19. Article
  20. FAK: A Potential Target for Cancer Therapy.ACS medicinal chemistry letters · 2025
    Article

99 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Jin ZhouKey Laboratory of Biorheological Science and Technology, Ministry of Education, College of Bioengineering, Chongqing University, Chongqing, 400044, China.
Qian YiDepartment of Physiology, School of Basic Medical Sciences, Southwest Medical University, Luzhou, 646000, Sichuan, China. yiqian2010@yeah.net.
Liling TangKey Laboratory of Biorheological Science and Technology, Ministry of Education, College of Bioengineering, Chongqing University, Chongqing, 400044, China. tangliling@cqu.edu.cn.
Chongqing University · CNSouthwest Medical University · CN

Funding

Fundamental Research Funds for Central Universities of the Central South University (CN) No.2018CDYJSY0055; Fundamental Research Funds for Central Universities of the Central South University (CN)2018CQDYSG0021the Natural Science Foundation of China No.31670952
6 · The paper itself

Abstract

FAK is a tyrosine kinase overexpressed in cancer cells and plays an important role in the progression of tumors to a malignant phenotype. Except for its typical role as a cytoplasmic kinase downstream of integrin and growth factor receptor signaling, related studies have shown new aspects of the roles of FAK in the nucleus. FAK can promote p53 degradation through ubiquitination, leading to cancer cell growth and proliferation. FAK can also regulate GATA4 and IL-33 expression, resulting in reduced inflammatory responses and immune escape. These findings establish a new model of FAK from the cytoplasm to the nucleus. Activated FAK binds to transcription factors and regulates gene expression. Inactive FAK synergizes with different E3 ligases to promote the turnover of transcription factors by enhancing ubiquitination. In the tumor microenvironment, nuclear FAK can regulate the formation of new blood vessels, affecting the tumor blood supply. This article reviews the roles of nuclear FAK in regulating gene expression. In addition, the use of FAK inhibitors to target nuclear FAK functions will also be emphasized.

Indexed as

AnimalsAntineoplastic AgentsCell Line, TumorCell NucleusCell ProliferationCytoplasmFocal Adhesion Protein-Tyrosine KinasesHumansMolecular Targeted TherapyNeoplasmsProtein Kinase InhibitorsProtein TransportSignal TransductionAntineoplastic AgentsFocal Adhesion Protein-Tyrosine KinasesProtein Kinase InhibitorsCancerGene expressionInhibitorsNuclear FAKTranscription factors

Identifiers

PMID31186061
PMCPMC6560741
OpenAlexW2949922878

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.