Evidence map›Paper›PMID 27285763›Full record

ArticleOncotarget2016

Increased cancer stem cell invasion is mediated by myosin IIB and nuclear translocation.

Dustin Thomas, Praveena S Thiagarajan, Vandana Rai, Ofer Reizes, Justin Lathia, Thomas Egelhoff

Abstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–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

12 citing papers in PubMed.

  1. Regulation of Notch signaling by non-muscle myosin II Zipper in Drosophila.Cellular and molecular life sciences : CMLS · 2024
    Article
  2. Article
  3. SFRP1 induces a stem cell phenotype in prostate cancer cells.Frontiers in cell and developmental biology · 2023
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Transcriptomic analysis reveals that BMP4 sensitizes glioblastoma tumor-initiating cells to mechanical cues.Matrix biology : journal of the International Society for Matrix Biology · 2020
    Article
  9. Article
  10. Review
  11. Roles of Wnt Target Genes in the Journey of Cancer Stem Cells.International journal of molecular sciences · 2017
    Review
  12. 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.

Dustin ThomasDepartment of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Praveena S ThiagarajanDepartment of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Vandana RaiDepartment of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Ofer ReizesDepartment of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Justin LathiaDepartment of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Thomas EgelhoffDepartment of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.

Funding

Myosin Assembly in DictyosteliumR01GM050009 · NIGMS · CLEVELAND CLINIC LERNER COM-CWRU · PI EGELHOFF, THOMAS · 1998 to 2017
$4.7M
Cell-cell communication in CSC self renewal and breast cancer progressionR21CA191263 · NCI · CLEVELAND CLINIC LERNER COM-CWRU · PI LATHIA, JUSTIN D., REIZES, OFER · 2015 to 2016
$379k
NCI NIH HHS R21 CA191263NIGMS NIH HHS R01 GM050009
6 · The paper itself

Abstract

Despite many advances in the treatment of breast cancer, it remains one of the leading causes of death among women. One hurdle for effective therapy is the treatment of the highly invasive and tumorigenic subpopulation of tumors called cancer stem cells (CSCs). CSCs, when stimulated with EGF, migrate through a physiological 3D collagen matrix at a higher velocity than non-stem cancer cells (non-SCCs). This increased invasion is due, in part, by an enhanced nuclear translocation ability of CSCs. We observed no difference between CSC and non-SCC in cellular migration rates on a 2D surface. Furthermore, during transwell migration using large diameter transwell pores, both CSC and non-SCC populations migrated with similar efficiency. However, when challenged with more restrictive transwells, CSCs were dramatically more capable of transwell migration. These results implicate nuclear translocation as a major rate limiting factor for CSC dissemination. We further show that non-muscle myosin IIB is critical for this enhanced nuclear translocation and the ability for cancer stem cells to efficiently migrate through restrictive 3D environments. These studies suggest that cytoskeletal elements upregulated in CSCs, such as myosin IIB, may be valuable targets for intervention in cancer stem cell dispersal from tumors.

Indexed as

Active Transport, Cell NucleusCell Line, TumorCell MovementCell NucleusHumansNeoplasm InvasivenessNeoplastic Stem CellsNonmuscle Myosin Type IIBNonmuscle Myosin Type IIBbreast cancercancer stem cellinvasionmyosin IIBnuclear translocation

Identifiers

PMID27285763
PMCPMC5216963

What OpenQuestion holds

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LicenceCC BY
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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.