Evidence map›Paper›PMID 23351358›Full record

ArticleBMC cancer2013

Cytostasis and morphological changes induced by mifepristone in human metastatic cancer cells involve cytoskeletal filamentous actin reorganization and impairment of cell adhesion dynamics.

BreeAnn N Brandhagen, Chelsea R Tieszen, Tara M Ulmer, Maria S Tracy, Alicia A Goyeneche, Carlos M Telleria

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.3field-weighted citation impact, top 14% 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

20 citing papers in PubMed, 53 citations in OpenAlex.

  1. Effect of Mifepristone on Migration and Proliferation of Oral Cancer Cells.International journal of molecular sciences · 2024
    Article
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  3. Dipeptidyl Peptidase 4/Midline-1 Axis Promotes T Lymphocyte Motility in Atherosclerosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
  4. Article
  5. The diverse functions of FAT1 in cancer progression: good, bad, or ugly?Journal of experimental & clinical cancer research : CR · 2022
    Review
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  13. ExploitingEXCLI journal · 2018
    Article
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  18. Article
  19. Antiprogestins in gynecological diseases.Reproduction (Cambridge, England) · 2015
    Review
  20. 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

6 authors at 1 institution in 1 country.

BreeAnn N BrandhagenDivision of Basic Biomedical Science, Sanford School of Medicine of The University of South Dakota, 414 East Clark Street, Vermillion, SD 57069, USA.
Chelsea R Tieszen
Tara M Ulmer
Maria S Tracy
Alicia A Goyeneche
Carlos M Telleria
University of South Dakota · US

Funding

Growth Inhibition Induced by Mifepristone in Ovarian CancerK22CA121991 · NCI · UNIVERSITY OF SOUTH DAKOTA · PI TELLERIA, CARLOS MARCELO · 2007 to 2009
$525k
Antiprogestin therapy for ovarian cancerR15CA164622 · NCI · UNIVERSITY OF SOUTH DAKOTA · PI TELLERIA, CARLOS MARCELO · 2012 to 2012
$426k
NCI NIH HHS K22 CA121991NCI NIH HHS K22CA121991NCI NIH HHS K22CA121991-S1NCI NIH HHS R15 CA164622NCI NIH HHS R15CA164622
6 · The paper itself

Abstract

backgroundChanges in cell shape and plasticity in cytoskeletal dynamics are critically involved in cell adhesion, migration, invasion and the overall process of metastasis. Previous work in our laboratory demonstrated that the synthetic steroid mifepristone inhibited the growth of highly metastatic cancer cells, while simultaneously causing striking changes in cellular morphology. Here we assessed whether such morphological alterations developed in response to cytostatic concentrations of mifepristone are reversible or permanent, involve rearrangement of cytoskeletal proteins, and/or affect the adhesive capacity of the cells.

methodsCancer cell lines of the ovary (SKOV-3), breast (MDA-MB-231), prostate (LNCaP), and nervous system (U87MG) were exposed to cytostatic concentrations of mifepristone and studied by phase-contrast microscopy. The transient or permanent nature of the cytostasis and morphological changes caused by mifepristone was assessed, as well as the rearrangement of cytoskeletal proteins. De-adhesion and adhesion assays were utilized to determine if mifepristone-arrested and morphologically dysregulated cells had abnormal de-adhesion/adhesion dynamics when compared to vehicle-treated controls.

resultsMifepristone-treated cells displayed a long, thin, spindle-like shape with boundaries resembling those of loosely adhered cells. Growth arrest and morphology changes caused by mifepristone were reversible in SKOV-3, MDA-MB-231 and U87MG, but not in LNCaP cells that instead became senescent. All cancer cell types exposed to mifepristone displayed greatly increased actin ruffling in association with accelerated de-adhesion from the culture plate, and delayed adhesion capacity to various extracellular matrix components.

conclusionsCytostatic concentrations of mifepristone induced alterations in the cellular structure of a panel of aggressive, highly metastatic cancer cells of different tissues of origin. Such changes were associated with re-distribution of actin fibers that mainly form non-adhesive membrane ruffles, leading to dysregulated cellular adhesion capacity.

Indexed as

Actin CytoskeletonAntineoplastic Agents, HormonalBreast NeoplasmsCell AdhesionCell Line, TumorCell ProliferationCell ShapeCytostatic AgentsFemaleHormone AntagonistsHumansMaleMifepristoneNeoplasm InvasivenessNeoplasmsNervous System NeoplasmsAntineoplastic Agents, HormonalCytostatic AgentsHormone AntagonistsMifepristone

Identifiers

PMID23351358
PMCPMC3562154
OpenAlexW1997410580

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.