Evidence map›Paper›PMID 22383427›Full record

ArticleEndocrine-related cancer2012

Sorafenib decreases proliferation and induces apoptosis of prostate cancer cells by inhibition of the androgen receptor and Akt signaling pathways.

Su Jung Oh, Holger H H Erb, Alfred Hobisch, Frédéric R Santer, Zoran Culig

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Endocrine-related cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

38 citing papers in PubMed, 64 citations in OpenAlex.

  1. Copy Number Changes Are Associated with Response to Treatment with Carboplatin, Paclitaxel, and Sorafenib in Melanoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016
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  17. Interleukin-27 augments the inhibitory effects of sorafenib on bladder cancer cells.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2017
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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 2 institutions in 1 country.

Su Jung OhDivision of Experimental Urology, Department of Urology, Innsbruck Medical University, Anichstrasse 35, A-6020 Innsbruck, Austria.
Holger H H Erb
Alfred Hobisch
Frédéric R Santer
Zoran Culig
Innsbruck Medical University · ATLandeskrankenhaus Feldkirch · AT

Funding

Austrian Science Fund FWF W 1101
6 · The paper itself

Abstract

Antihormonal and chemotherapy are standard treatments for nonorgan-confined prostate cancer. The effectivity of these therapies is limited and the development of alternative approaches is necessary. In the present study, we report on the use of the multikinase inhibitor sorafenib in a panel of prostate cancer cell lines and their derivatives which mimic endocrine and chemotherapy resistance. (3)H-thymidine incorporation assays revealed that sorafenib causes a dose-dependent inhibition of proliferation of all cell lines associated with downregulation of cyclin-dependent kinase 2 and cyclin D1 expression. Apoptosis was induced at 2  μM of sorafenib in androgen-sensitive cells, whereas a higher dose of the drug was needed in castration-resistant cell lines. Sorafenib stimulated apoptosis in prostate cancer cell lines through downregulation of myeloid cell leukemia-1 (MCL-1) expression and Akt phosphorylation. Although concentrations of sorafenib required for the antitumor effect in therapy-resistant sublines were higher than those needed in parental cells, the drug showed efficacy in cells which became resistant to bicalutamide and docetaxel respectively. Most interestingly, we show that sorafenib has an inhibitory effect on androgen receptor (AR) and prostate-specific antigen expression. In cells in which AR expression was downregulated by short interfering RNA, the treatment with sorafenib increased apoptosis in an additive manner. In summary, the results of the present study indicate that there is a potential to use sorafenib in prostate cancers as an adjuvant therapy option to current androgen ablation treatments, but also in progressed prostate cancers that become unresponsive to standard therapies.

Indexed as

Androgen Receptor AntagonistsAntineoplastic AgentsApoptosisBenzenesulfonatesCaspase 3Caspase 7Cell Line, TumorCell ProliferationCyclin D1Cyclin-Dependent Kinase 2Down-RegulationHumansMaleMyeloid Cell Leukemia Sequence 1 ProteinNiacinamidePhenylurea CompoundsAndrogen Receptor AntagonistsAntineoplastic AgentsAR protein, humanBenzenesulfonatesCaspase 3Caspase 7Cdk2 protein, mouseCyclin D1Cyclin-Dependent Kinase 2Mcl1 protein, mouseMyeloid Cell Leukemia Sequence 1 ProteinNiacinamidePhenylurea CompoundsProstate-Specific AntigenProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2PyridinesReceptors, AndrogenRNA, Small InterferingSorafenib

Identifiers

PMID22383427
PMCPMC3353237
OpenAlexW2120468822

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.