Evidence map›Paper›PMID 25013907›Full record

ArticlePloS one2014

Association of toxicity of sorafenib and sunitinib for human keratinocytes with inhibition of signal transduction and activator of transcription 3 (STAT3).

Kazuhiro Yamamoto, Atsushi Mizumoto, Kohji Nishimura, Atsushi Uda, Akira Mukai, Kazuhiko Yamashita, Manabu Kume, Hiroo Makimoto, Toshinori Bito, Chikako Nishigori and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

13 citing papers in PubMed, 33 citations in OpenAlex.

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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

13 authors at 2 institutions in 1 country.

Kazuhiro YamamotoDepartment of Pharmacy, Kobe University Hospital, Kobe, Japan.
Atsushi MizumotoDivision of Pharmacokinetics, Kobe University Graduate School of Medicine, Kobe, Japan.
Kohji NishimuraDivision of Pharmacokinetics, Kobe University Graduate School of Medicine, Kobe, Japan.
Atsushi UdaDepartment of Pharmacy, Kobe University Hospital, Kobe, Japan.
Akira MukaiDepartment of Pharmacy, Kobe University Hospital, Kobe, Japan.
Kazuhiko YamashitaDepartment of Pharmacy, Kobe University Hospital, Kobe, Japan.
Manabu KumeDepartment of Pharmacy, Kobe University Hospital, Kobe, Japan.
Hiroo MakimotoDepartment of Pharmacy, Kobe University Hospital, Kobe, Japan.
Toshinori BitoDivision of Dermatology, Kobe University Graduate School of Medicine, Kobe, Japan.
Chikako NishigoriDivision of Dermatology, Kobe University Graduate School of Medicine, Kobe, Japan.
Tsutomu NakagawaDepartment of Pharmacy, Kobe University Hospital, Kobe, Japan; Division of Pharmacokinetics, Kobe University Graduate School of Medicine, Kobe, Japan.
Takeshi HiranoDepartment of Pharmacy, Kobe University Hospital, Kobe, Japan; Division of Pharmacokinetics, Kobe University Graduate School of Medicine, Kobe, Japan.
Midori HiraiDepartment of Pharmacy, Kobe University Hospital, Kobe, Japan; Division of Pharmacokinetics, Kobe University Graduate School of Medicine, Kobe, Japan.
Kobe University Hospital · JPKobe University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hand-foot skin reaction is a most common multi-kinase inhibitor-related adverse event. This study aimed to examine whether the toxicity of sorafenib and sunitinib for human keratinocytes was associated with inhibiting signal transduction and activator of transcription 3 (STAT3). We studied whether STAT3 activity affects sorafenib- and sunitinib-induced cell growth inhibition in HaCaT cells by WST-8 assay. Stattic enhanced the cell-growth inhibitory and apoptotic effects of sorafenib and sunitinib. HaCaT cells transfected with constitutively-active STAT3 (STAT3C) were resistant to the sorafenib- and sunitinib-induced cell growth inhibition. STAT3 activity decreased after short-term treatment with sorafenib and sunitinib in a dose-dependent manner and recovered after long-term treatment with sorafenib and sunitinib at low doses. Moreover, the expression of survivin and bcl-2 decreased after treatment with sorafenib and sunitinib was concomitant with variations in STAT3 activity. Sorafenib-induced STAT3 inhibition was mediated by regulation via MAPK pathways in HaCaT cells, while sunitinib-induced STAT3 inhibition was not. Thus, STAT3 activation mediating apoptosis suppressors may be a key factor in sorafenib and sunitinib-induced keratinocyte cytotoxicity.

Indexed as

Antineoplastic AgentsCell Line, TransformedCell ProliferationCyclic S-OxidesGene Expression RegulationHumansIndolesInhibitor of Apoptosis ProteinsKeratinocytesMitogen-Activated Protein KinasesNiacinamidePhenylurea CompoundsProtein Kinase InhibitorsProto-Oncogene Proteins c-bcl-2PyrrolesSignal Transduction2-(2-methoxy-4-nitrophenyl)-3-(4-nitrophenyl)-5-(2,4-disulfophenyl)-2H tetrazolium monosodium saltAntineoplastic AgentsBIRC5 protein, humanCyclic S-OxidesIndolesInhibitor of Apoptosis ProteinsMitogen-Activated Protein KinasesNiacinamidePhenylurea CompoundsProtein Kinase InhibitorsProto-Oncogene Proteins c-bcl-2PyrrolesSorafenibSTAT3 protein, humanSTAT3 Transcription FactorstatticSunitinibSurvivinTetrazolium Salts

Identifiers

PMID25013907
PMCPMC4094497
OpenAlexW2083281295

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.