Evidence map›Paper›PMID 23665680›Full record

ArticleOncogene2014

Met-induced membrane blebbing leads to amoeboid cell motility and invasion.

A Laser-Azogui, T Diamant-Levi, S Israeli, Y Roytman, I Tsarfaty

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

31 citing papers in PubMed, 46 citations in OpenAlex.

  1. Moesin is an αCellular and molecular life sciences : CMLS · 2026
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  11. Chemokine-biased robust self-organizing polarization of migrating cells in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  12. Review
  13. Actin cytoskeleton in mesenchymal-to-amoeboid transition of cancer cells.International review of cell and molecular biology · 2020
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Identification of a combined biomarker for malignant transformation in oral submucous fibrosis.Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2017
    Article
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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

5 authors at 1 institution in 1 country.

A Laser-AzoguiDepartment of Clinical Microbiology and Immunology, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
T Diamant-LeviDepartment of Clinical Microbiology and Immunology, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
S IsraeliDepartment of Clinical Microbiology and Immunology, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
Y RoytmanDepartment of Clinical Microbiology and Immunology, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
I TsarfatyDepartment of Clinical Microbiology and Immunology, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
Tel Aviv University · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Met tyrosine kinase has been implicated in tumorigenesis and metastasis; its overexpression and deregulation is often observed in cancer. Although Met's functions in cell motility has been studied extensively, its involvement in bleb-based, amoeboid motility is yet to be determined. The aim of this work is to study the role of Met in amoeboid cell motility and invasion. We show that aggressive breast cancer cells expressing high levels of endogenous Met, as well as HEK293T cells over expressing fluorescent Met, exhibit constitutive, ligand-independent Met activation, leading to Met-dependent membrane blebbing and amoeboid cell motility; HEK293T cells over expressing fluorescent Met were able to invade in three-dimensional matrix. Hyper-activated Met mutant significantly enhances blebbing and cell motility. Met inhibition by either a Met-specific inhibitor or by exogenous expression of a dominant-negative Met remarkably repressed membrane blebbing and invasion. Inhibition of Rho signaling pathway by a ROCK inhibitor also represses Met-induced blebbing, suggesting that Met regulates the blebbing machinery through Rho-ROCK pathway, which controls the actin-myosin contractile force. Either de-polymerization or hyper-polymerization of the actin cytoskeleton abrogates Met-induced blebbing, signifying that actin polymerization has a role in halting and retracting Met-induced mature blebs. Indeed, when blebs retract, membrane wrinkles containing high levels of Met and actin are generated, indicating localized formation of Met-signaling microdomains. We suggest that this bleb-based activity is induced by amplification of Met signaling in unique membrane domains generated by bleb retraction. Our results indicate that Met-induced blebbing has an important role in cell detachment, amoeboid motility and invasion ability, which are utilized by cancer cells for migration and metastasis.

Indexed as

Gene Expression Regulation, NeoplasticActin CytoskeletonActinsApoptosisBreast NeoplasmsCell Line, TumorCell MembraneCell MovementHEK293 CellsHumansMembrane MicrodomainsMyosinsNeoplasm InvasivenessNeoplasm MetastasisProtein Structure, TertiaryProto-Oncogene Proteins c-metActinsMET protein, humanMyosinsProto-Oncogene Proteins c-met

Identifiers

PMID23665680
OpenAlexW2073621719

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.