Evidence map›Paper›PMID 25594058›Full record

ArticleOncoscience2014

Rac1 as a multifunctional therapeutic target to prevent and combat cancer metastasis.

Christoph R Arnold, Alshaimaa Abdelmoez, Gudrun Thurner, Paul Debbage, Peter Lukas, Sergej Skvortsov, Ira-Ida Skvortsova

Open access · bronzeAbstract read
In one paragraph

Article in Oncoscience, 2014. 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
1.3field-weighted citation impact, top 20% 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

12 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Rac1, A Potential Target for Tumor Therapy.Frontiers in oncology · 2021
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
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

7 authors at 1 institution in 2 countries.

Christoph R ArnoldLaboratory for Experimental and Translational Research on Radiation Oncology (EXTRO-Lab), Dept. of Therapeutic Radiology and Oncology, Innsbruck Medical University, Innsbruck, Austria.
Alshaimaa AbdelmoezDepartment of Anatomy, Histology and Embryology, Innsbruck Medical University, Innsbruck, Austria.
Gudrun ThurnerDepartment of Anatomy, Histology and Embryology, Innsbruck Medical University, Innsbruck, Austria.
Paul DebbageDepartment of Anatomy, Histology and Embryology, Innsbruck Medical University, Innsbruck, Austria.
Peter LukasLaboratory for Experimental and Translational Research on Radiation Oncology (EXTRO-Lab), Dept. of Therapeutic Radiology and Oncology, Innsbruck Medical University, Innsbruck, Austria.
Sergej Skvortsov *Laboratory for Experimental and Translational Research on Radiation Oncology (EXTRO-Lab), Dept. of Therapeutic Radiology and Oncology, Innsbruck Medical University, Innsbruck, Austria.
Ira-Ida Skvortsova *Laboratory for Experimental and Translational Research on Radiation Oncology (EXTRO-Lab), Dept. of Therapeutic Radiology and Oncology, Innsbruck Medical University, Innsbruck, Austria.
Innsbruck Medical University · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metastatic progression of malignant tumors resistant to conventional therapeutic approaches is an ultimate challenge in clinical oncology. Despite the efforts of basic and clinical researchers, there is still no effective treatment schedule to prevent or combat metastatic spread of malignant tumors. This report presents recent findings that could help in the development of targeted therapeutics directed against the most aggressive and treatment-resistant carcinoma cells. It was demonstrated that HNSCC carcinoma cell lines with acquired treatment resistance possessed increased number of cells with carcinoma stem cell (CSC) properties. Furthermore, resistant cells were characterized by increased expression of Rac1, enhanced cell migration, and accelerated release of proangio- and vasculogenic factors (VEGF-A) and influence on endothelial cell (HMEC-1) migration. Inhibition of Rac1 signaling in the treatment-resistant carcinoma cells can interrupt metastatic process due to anoikis restoration and decrease of cell migration. It is also suggested that carcinoma cells with repressed survival capacities will be characterized by reduced release of proangiogenic factors, resulting in the decrease of endothelial cell migration. Therefore targeting of Rac1-related pathways may be considered as a promising therapeutic approach to prevent or combat metastatic lesions.

Indexed as

carcinoma stem cellshead and neck squamous cell carcinomametastasisRac1treatment resistance

Identifiers

PMID25594058
PMCPMC4278326
OpenAlexW2183996639

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.