Evidence map›Paper›PMID 23455323›Full record

ArticleOncogene2014

Mutant B-RAF-Mcl-1 survival signaling depends on the STAT3 transcription factor.

T M Becker, S C Boyd, B Mijatov, K Gowrishankar, S Snoyman, G M Pupo, R A Scolyer, G J Mann, R F Kefford, X D Zhang and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

35 citing papers in PubMed, 68 citations in OpenAlex.

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  12. Aberrant expression of the COX2/PGEScientific reports · 2020
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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

11 authors at 5 institutions in 1 country.

T M BeckerWestmead Institute for Cancer Research, University of Sydney at Westmead Millennium Institute, Westmead Hospital, Sydney, New South Wales, Australia.
S C BoydWestmead Institute for Cancer Research, University of Sydney at Westmead Millennium Institute, Westmead Hospital, Sydney, New South Wales, Australia.
B MijatovWestmead Institute for Cancer Research, University of Sydney at Westmead Millennium Institute, Westmead Hospital, Sydney, New South Wales, Australia.
K GowrishankarWestmead Institute for Cancer Research, University of Sydney at Westmead Millennium Institute, Westmead Hospital, Sydney, New South Wales, Australia.
S SnoymanWestmead Institute for Cancer Research, University of Sydney at Westmead Millennium Institute, Westmead Hospital, Sydney, New South Wales, Australia.
G M PupoWestmead Institute for Cancer Research, University of Sydney at Westmead Millennium Institute, Westmead Hospital, Sydney, New South Wales, Australia.
R A ScolyerMelanoma Institute Australia, Sydney, New South Wales, Australia.
G J Mann1] Westmead Institute for Cancer Research, University of Sydney at Westmead Millennium Institute, Westmead Hospital, Sydney, New South Wales, Australia [2] Melanoma Institute Australia, Sydney, New South Wales, Australia.
R F Kefford1] Westmead Institute for Cancer Research, University of Sydney at Westmead Millennium Institute, Westmead Hospital, Sydney, New South Wales, Australia [2] Melanoma Institute Australia, Sydney, New South Wales, Australia.
X D ZhangImmunology and Oncology Unit, University of Newcastle, Newcastle, New South Wales, Australia.
H RizosWestmead Institute for Cancer Research, University of Sydney at Westmead Millennium Institute, Westmead Hospital, Sydney, New South Wales, Australia.
Westmead Hospital · AUWestmead Institute · AUMelanoma Institute Australia · AUThe University of Sydney · AUUniversity of Newcastle Australia · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Approximately 50% of melanomas depend on mutant B-RAF for proliferation, metastasis and survival. The inhibition of oncogenic B-RAF with highly targeted compounds has produced remarkable albeit short-lived clinical responses in B-RAF mutant melanoma patients. Reactivation of signaling downstream of B-RAF is frequently associated with acquired resistance to B-RAF inhibitors, and the identification of B-RAF targets may provide new strategies for managing melanoma. Oncogenic B-RAF(V600E) is known to promote the stabilizing phosphorylation of the anti-apoptotic protein Mcl-1, implicated in melanoma survival and chemoresistance. We now show that B-RAF(V600E) signaling also induces the transcription of Mcl-1 in melanocytes and melanoma. We demonstrate that activation of STAT3 serine-727 and tyrosine-705 phosphorylations is promoted by B-RAF(V600E) activity and that the Mcl-1 promoter is dependent on a STAT consensus-site for B-RAF-mediated activation. Consequently, suppression of STAT3 activity disrupted B-RAF(V600E)-mediated induction of Mcl-1 and reduced melanoma cell survival. We propose that STAT3 has a central role in the survival and contributes to chemoresistance of B-RAF(V600E) melanoma.

Indexed as

Cell Line, TumorCell SurvivalHumansInterleukin-6MelanocytesMelanomaMutationMyeloid Cell Leukemia Sequence 1 ProteinPhosphorylationPromoter Regions, GeneticProto-Oncogene Proteins B-rafSignal TransductionSTAT3 Transcription FactorTranscriptional ActivationTranscription FactorsBRAF protein, humanIL6 protein, humanInterleukin-6MCL1 protein, humanMyeloid Cell Leukemia Sequence 1 ProteinProto-Oncogene Proteins B-rafSTAT3 protein, humanSTAT3 Transcription FactorTranscription Factors

Identifiers

PMID23455323
OpenAlexW1973304938

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.