Evidence map›Paper›PMID 16170368›Full record

ArticleOncogene2005

Resensitization of breast cancer cells to anoikis by tropomyosin-1: role of Rho kinase-dependent cytoskeleton and adhesion.

Shantaram Bharadwaj, Ruchi Thanawala, Giulia Bon, Rita Falcioni, G L Prasad

Abstract read
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In one paragraph

Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
2.8field-weighted citation impact, top 11% 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

46 citing papers in PubMed, 91 citations in OpenAlex.

  1. Review
  2. FERMT2 drives anoikis resistance and peritoneal metastasis by enhancing extracellular matrix deposition in gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2025
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  5. NCell death and differentiation · 2023
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  12. Cell death pathways and viruses: Role of microRNAs.Molecular therapy. Nucleic acids · 2021
    Review
  13. Article
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  15. Article
  16. A Tale of Two States: Normal and Transformed, With and Without Rigidity Sensing.Annual review of cell and developmental biology · 2019
    Review
  17. Article
  18. Article
  19. 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

5 authors at 3 institutions in 3 countries.

Shantaram BharadwajDepartment of General Surgery, Wake Forest University School of Medicine, Medical Center Blvd., Winston-Salem, NC 27157, USA.
Ruchi Thanawala
Giulia Bon
Rita Falcioni
G L Prasad
Wake Forest University · USCancer Institute (WIA) · INNational Cancer Institute · MY

Funding

Intramural NIH HHS
6 · The paper itself

Abstract

Two most common properties of malignant cells are the presence of aberrant actin cytoskeleton and resistance to anoikis. Suppression of several key cytoskeletal proteins, including tropomyosin-1 (TM1), during neoplastic transformation is hypothesized to contribute to the altered cytoskeleton and neoplastic phenotype. Using TM1 as a paradigm, we have shown that cytoskeletal proteins induce anoikis in breast cancer (MCF-7 and MDA MB 231) cells. Here, we have tested the hypothesis that TM1-mediated cytoskeletal changes regulate integrin activity and the sensitivity to anoikis. TM1 expression in MDA MB 231 cells promotes the assembly of stress fibers, induces rapid anoikis via caspase-dependent pathways involving the release of cytochrome c. Further, TM1 inhibits binding of MDA MB 231 cells to collagen I, but promotes adhesion to laminin. Inhibition of Rho kinase disrupts TM1-mediated cytoskeletal reorganization and adhesion to the extracellular matrix components, whereas the parental cells attach to collagen I, spread and form extensive actin meshwork in the presence of Rho kinase inhibitor, underscoring the differences in parental and TM1-transduced breast cancer cells. Further, treatment with the cytoskeletal disrupting drugs rescues the cells from TM1-induced anoikis. These new findings demonstrate that the aberrant cytoskeleton contributes to neoplastic transformation by conferring resistance to anoikis. Restoration of stress fiber network through enhanced expression of key cytoskeletal proteins may modulate the activity of focal adhesions and sensitize the neoplastic cells to anoikis.

Indexed as

Drug Resistance, NeoplasmActin CytoskeletonAnoikisBreast NeoplasmsCaspasesCell AdhesionCell Line, TumorCell ProliferationCytoskeletonExtracellular MatrixFemaleHumansIntegrinsIntracellular Signaling Peptides and ProteinsProtein Serine-Threonine Kinasesrho-Associated KinasesCaspasesIntegrinsIntracellular Signaling Peptides and ProteinsProtein Serine-Threonine Kinasesrho-Associated KinasesTPM1 protein, humanTropomyosin

Identifiers

PMID16170368
OpenAlexW1985035975

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.