Evidence map›Paper›PMID 24509905›Full record

ArticleCancer research2014

Cofilin drives cell-invasive and metastatic responses to TGF-β in prostate cancer.

Joanne Collazo, Beibei Zhu, Spencer Larkin, Sarah K Martin, Hong Pu, Craig Horbinski, Shahriar Koochekpour, Natasha Kyprianou

Erratum issuedAbstract read
In one paragraph

Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 59 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

59 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. Role of actin-binding proteins in prostate cancer.Frontiers in cell and developmental biology · 2024
    Review
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  20. Alterations in TGFβ signaling during prostate cancer progression.American journal of clinical and experimental urology · 2021
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors.

Joanne CollazoAuthors' Affiliations: Departments of Toxicology, Urology, Molecular and Cellular Biochemistry, and Pathology, University of Kentucky College of Medicine, Lexington, Kentucky; and Departments of Cancer Genetics and Urology, Roswell Park Cancer Institute, Buffalo, New York.
Beibei Zhu
Spencer Larkin
Sarah K Martin
Hong Pu
Craig Horbinski
Shahriar Koochekpour
Natasha Kyprianou

Funding

University of Kentucky Markey Cancer Center Support Grant ECIA SupplementP30CA177558 · NCI · UNIVERSITY OF KENTUCKY · PI Jennifer F Rogers · 2013 to 2026
$38.3M
UNDERSTANDING THE MOLECULAR BASIS OF EPIGENETIC TRANSCRIPTIONAL SILENCINGP20RR020171 · NCRR · UNIVERSITY OF KENTUCKY · PI WATT, DAVID · 2004 to 2011
$16.5M
TGF-Beta Signaling Effectors in Prostate Growth Regulation/Tumor ProgressionR01DK083761 · NIDDK · UNIVERSITY OF KENTUCKY · PI KYPRIANOU, NATASHA · 2010 to 2013
$1.3M
The Significance of Isocitrate Dehydrogenase Mutations in GliomasK08CA155764 · NCI · UNIVERSITY OF KENTUCKY · PI HORBINSKI, CRAIG MICHAEL · 2011 to 2015
$857k
NCI NIH HHS CA155764NCI NIH HHS K08 CA155764NCI NIH HHS P30 CA177558NCRR NIH HHS 2P20 RR020171NCRR NIH HHS P20 RR020171NIDDK NIH HHS R01 DK083761
6 · The paper itself

Abstract

Cofilin (CFL) is an F-actin-severing protein required for the cytoskeleton reorganization and filopodia formation, which drives cell migration. CFL binding and severing of F-actin is controlled by Ser3 phosphorylation, but the contributions of this step to cell migration during invasion and metastasis of cancer cells are unclear. In this study, we addressed the question in prostate cancer cells, including the response to TGF-β, a critical regulator of migration. In cells expressing wild-type CFL, TGF-β treatment increased LIMK-2 activity and cofilin phosphorylation, decreasing filopodia formation. Conversely, constitutively active CFL (SerAla) promoted filipodia formation and cell migration mediated by TGF-β. Notably, in cocultures of prostate cancer epithelial cells and cancer-associated fibroblasts, active CFL promoted invasive migration in response to TGF-β in the microenvironment. Further, constitutively active CFL elevated the metastatic ability of prostate cancer cells in vivo. We found that levels of active CFL correlated with metastasis in a mouse model of prostate tumor and that in human prostate cancer, CFL expression was increased significantly in metastatic tumors. Our findings show that the actin-severing protein CFL coordinates responses to TGF-β that are needed for invasive cancer migration and metastasis.

Indexed as

Actin Depolymerizing FactorsAnimalsCell Line, TumorCell MovementDisease Models, AnimalHeterograftsHumansMaleMiceMice, TransgenicNeoplasm InvasivenessNeoplasm MetastasisPhosphorylationProstatic NeoplasmsSignal TransductionTransforming Growth Factor betaActin Depolymerizing FactorsTransforming Growth Factor beta

Identifiers

PMID24509905
PMCPMC4488067

What OpenQuestion holds

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Registered trials

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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.