Evidence map›Paper›PMID 25309914›Full record

ArticleBioMed research international2014

Biological and molecular effects of small molecule kinase inhibitors on low-passage human colorectal cancer cell lines.

Falko Lange, Benjamin Franz, Claudia Maletzki, Michael Linnebacher, Maja Hühns, Robert Jaster

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
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  9. Application ofOncotarget · 2017
    Article
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  13. Article
  14. Biology of colorectal cancer.Ecancermedicalscience · 2015
    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

6 authors at 1 institution in 1 country.

Falko LangeDepartment of Medicine II, Division of Gastroenterology, Rostock University Medical Center, Ernst-Heydemann-Straße 6, 18057 Rostock, Germany ; Oscar Langendorff Institute of Physiology, Rostock University Medical Center, Gertrudenstraße 9, 18057 Rostock, Germany.
Benjamin FranzDepartment of Medicine II, Division of Gastroenterology, Rostock University Medical Center, Ernst-Heydemann-Straße 6, 18057 Rostock, Germany.
Claudia MaletzkiMolecular Oncology and Immunotherapy, Department of General Surgery, Rostock University Medical Center, Schillingallee 35, 18057 Rostock, Germany.
Michael LinnebacherMolecular Oncology and Immunotherapy, Department of General Surgery, Rostock University Medical Center, Schillingallee 35, 18057 Rostock, Germany.
Maja HühnsInstitute of Pathology, Rostock University Medical Center, Strempelstraße 14, 18055 Rostock, Germany.
Robert JasterDepartment of Medicine II, Division of Gastroenterology, Rostock University Medical Center, Ernst-Heydemann-Straße 6, 18057 Rostock, Germany.
University of Rostock · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Low-passage cancer cell lines are versatile tools to study tumor cell biology. Here, we have employed four such cell lines, established from primary tumors of colorectal cancer (CRC) patients, to evaluate effects of the small molecule kinase inhibitors (SMI) vemurafenib, trametinib, perifosine, and regorafenib in an in vitro setting. The mutant BRAF (V600E/V600K) inhibitor vemurafenib, but also the MEK1/2 inhibitor trametinib efficiently inhibited DNA synthesis, signaling through ERK1/2 and expression of genes downstream of ERK1/2 in BRAF mutant cells only. In case of the AKT inhibitor perifosine, three cell lines showed a high or intermediate responsiveness to the drug while one cell line was resistant. The multikinase inhibitor regorafenib inhibited proliferation of all CRC lines with similar efficiency and independent of the presence or absence of KRAS, BRAF, PIK3CA, and TP53 mutations. Regorafenib action was associated with broad-range inhibitory effects at the level of gene expression but not with a general inhibition of AKT or MEK/ERK signaling. In vemurafenib-sensitive cells, the antiproliferative effect of vemurafenib was enhanced by the other SMI. Together, our results provide insights into the determinants of SMI efficiencies in CRC cells and encourage the further use of low-passage CRC cell lines as preclinical models.

Indexed as

AgedAged, 80 and overBromodeoxyuridineCell DeathCell Line, TumorCell ProliferationColorectal NeoplasmsFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticGenes, NeoplasmHumansInhibitory Concentration 50MaleMolecular Targeted TherapyProtein Kinase InhibitorsBromodeoxyuridineProtein Kinase InhibitorsSmall Molecule Libraries

Identifiers

PMID25309914
PMCPMC4182691
OpenAlexW2015955448

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.