Evidence map›Paper›PMID 28260860›Full record

ArticleDrug design, development and therapy2017

Antiproliferation effect of imatinib mesylate on MCF7, T-47D tumorigenic and MCF 10A nontumorigenic breast cell lines via PDGFR-β, PDGF-BB, c-Kit and SCF genes.

Ali Kadivar, Behnam Kamalidehghan, Hamid Akbari Javar, Benyamin Karimi, Reihaneh Sedghi, Mohamed Ibrahim Noordin

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2017. 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
2.3field-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

12 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Cytotoxicity of bismuth(III) dithiocarbamate derivatives by promoting a mitochondrial-dependent apoptotic pathway and suppressing MCF-7 breast adenocarcinoma cell invasion.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2024
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Use of multitarget tyrosine kinase inhibitors to attenuate platelet-derived growth factor signalling in lung disease.European respiratory review : an official journal of the European Respiratory Society · 2017
    Review
  10. Article
  11. Article
  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 at 3 institutions in 2 countries.

Ali KadivarDepartment of Pharmacy, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia.
Behnam KamalidehghanDepartment of Pharmacy, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia.
Hamid Akbari JavarDepartment of Pharmaceutics, Faculty of Pharmacy, Tehran University of Medical Sciences (TUMS), Tehran, Iran.
Benyamin KarimiDepartment of Pharmacology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia.
Reihaneh SedghiFaculty of Medicine, Shiraz University of Medical Sciences (SUMS), Shiraz, Iran.
Mohamed Ibrahim NoordinDepartment of Pharmacy, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia.
University of Malaya · MYShiraz University of Medical Sciences · IRTehran University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent cancer molecular therapies are targeting main functional molecules to control applicable process of cancer cells. Attractive targets are established by receptor tyrosine kinases, such as platelet-derived growth factor receptors (PDGFRs) and c-Kit as mostly irregular signaling, which is due to either over expression or mutation that is associated with tumorigenesis and cell proliferation. Imatinib mesylate is a selective inhibitor of receptor tyrosine kinase, including PDGFR-β and c-Kit. In this research, we studied how imatinib mesylate would exert effect on MCF7 and T-47D breast cancer and MCF 10A epithelial cell lines, the gene and protein expression of PDGFR-β, c-Kit and their relevant ligands platelet-derived growth factor (PDGF)-BB and stem cell factor (SCF). The MTS assay was conducted in therapeutic relevant concentration of 2-10 µM for 96, 120 and 144 h treatment. In addition, apoptosis induction and cytostatic activity of imatinib mesylate were investigated with the terminal deoxynucleotidyl transferase dUTP nick end labeling TUNEL and cell cycle assays, respectively, in a time-dependent manner. Comparative real-time PCR and Western blot analysis were conducted to evaluate the expression and regulation of imatinib target genes and proteins. Our finding revealed that imatinib mesylate antiproliferation effect, apoptosis induction and cytostatic activity were significantly higher in breast cancer cell lines compared to MCF 10A. This effect might be due to the expression of PDGFR-β, PDGF-BB, c-Kit and SCF, which was expressed by all examined cell lines, except the T-47D cell line which was not expressed c-Kit. However, examined gene and proteins expressed more in cancer cell lines. Therefore, imatinib mesylate was more effective on them. It is concluded that imatinib has at least two potential targets in both examined breast cancer cell lines and can be a promising drug for targeted therapy to treat breast cancer.

Indexed as

Antineoplastic AgentsBreastBreast NeoplasmsCell CycleCell LineCell ProliferationDose-Response Relationship, DrugDrug Screening Assays, AntitumorHumansImatinib MesylateMCF-7 CellsMolecular StructureProto-Oncogene Proteins c-kitReceptor, Platelet-Derived Growth Factor betaReceptors, Platelet-Derived Growth FactorStem Cell FactorAntineoplastic AgentsImatinib MesylateProto-Oncogene Proteins c-kitReceptor, Platelet-Derived Growth Factor betaReceptors, Platelet-Derived Growth FactorStem Cell Factorbreast cancercell cycle analysiscell cycle arrestcomparative real-time PCRcytostatic activityGleevecnormal breast cell lineprotein expressiontyrosine kinase receptor

Identifiers

PMID28260860
PMCPMC5327915
OpenAlexW2591384181

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.