Evidence map›Paper›PMID 26206378›Full record

ReviewCellular and molecular life sciences : CMLS2015

p53 regulates cytoskeleton remodeling to suppress tumor progression.

Keigo Araki, Takahiro Ebata, Alvin Kunyao Guo, Kei Tobiume, Steven John Wolf, Keiko Kawauchi

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.3field-weighted citation impact, top 23% 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

28 citing papers in PubMed, 37 citations in OpenAlex.

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  13. Intratumoral budding and automated CD8-positive T-cell density in pretreatment biopsies can predict response to neoadjuvant therapy in rectal adenocarcinoma.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 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

6 authors at 4 institutions in 2 countries.

Keigo ArakiFrontiers of Innovative Research in Science and Technology, Konan University, 7-1-20 Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo, 650-0047, Japan.
Takahiro EbataFrontiers of Innovative Research in Science and Technology, Konan University, 7-1-20 Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo, 650-0047, Japan.
Alvin Kunyao GuoCancer and Stem Cell Biology Program, Duke-NUS Graduate Medical School, 8 College Road, Singapore, 169857, Singapore.
Kei TobiumeGraduate School of Biomedical and Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima, Hiroshima, 734-8553, Japan.
Steven John WolfMechanobiology Institute, National University of Singapore, T-Lab, 5A Engineering Drive 1, Singapore, 117411, Singapore.
Keiko KawauchiFrontiers of Innovative Research in Science and Technology, Konan University, 7-1-20 Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo, 650-0047, Japan. kawauchi@center.konan-u.ac.jp.
Konan University · JPNational University of Singapore · SGDuke-NUS Medical School · SGHiroshima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer cells possess unique characteristics such as invasiveness, the ability to undergo epithelial-mesenchymal transition, and an inherent stemness. Cell morphology is altered during these processes and this is highly dependent on actin cytoskeleton remodeling. Regulation of the actin cytoskeleton is, therefore, important for determination of cell fate. Mutations within the TP53 (tumor suppressor p53) gene leading to loss or gain of function (GOF) of the protein are often observed in aggressive cancer cells. Here, we highlight the roles of p53 and its GOF mutants in cancer cell invasion from the perspective of the actin cytoskeleton; in particular its reorganization and regulation by cell adhesion molecules such as integrins and cadherins. We emphasize the multiple functions of p53 in the regulation of actin cytoskeleton remodeling in response to the extracellular microenvironment, and oncogene activation. Such an approach provides a new perspective in the consideration of novel targets for anti-cancer therapy.

Indexed as

Actin CytoskeletonAnimalsCadherinsCell Adhesion MoleculesCell MovementCytoskeletonHumansIntegrinsMutationNeoplasmsrho GTP-Binding ProteinsTumor Suppressor Protein p53CadherinsCell Adhesion MoleculesIntegrinsrho GTP-Binding ProteinsTP53 protein, humanTumor Suppressor Protein p53Contractile forcesECM degradationFocal adhesion proteinsMechanotransductionMetastasisp53p63Rho GTPases

Identifiers

PMID26206378
PMCPMC11114009
OpenAlexW1443802381

What OpenQuestion holds

Textmetadata
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.