Evidence map›Paper›PMID 24954509›Full record

ArticleOncogene2015

HSF1 regulation of β-catenin in mammary cancer cells through control of HuR/elavL1 expression.

Shiuh-Dih Chou, Ayesha Murshid, Takanori Eguchi, Jianlin Gong, Stuart K Calderwood

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

68 citing papers in PubMed, 126 citations in OpenAlex.

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  12. Role of m6A writers, erasers and readers in cancer.Experimental hematology & oncology · 2022
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8 more citing papers are in PubMed but not listed here.

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.

Shiuh-Dih Chou *Department of Radiation Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA02215.
Ayesha Murshid *Department of Radiation Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA02215.
Takanori EguchiDepartment of Radiation Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA02215.
Jianlin GongBoston University Medical Center, Boston, MA02215.
Stuart K CalderwoodDepartment of Radiation Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA02215.
Beth Israel Deaconess Medical Center · USBoston Medical Center · US

Funding

TRANSMEMBRANE SIGNAL MODULATION BY HYPERTHERMIAR01CA047407 · NCI · DANA-FARBER CANCER INSTITUTE · PI CALDERWOOD, STUART KEITH · 1988 to 2014
$4.3M
Extracellular Hsp70 and hyperthermia in tumor therapyR01CA119045 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI CALDERWOOD, STUART KEITH · 2007 to 2016
$3.1M
Complex Role of HSF1 in Breast CancerR01CA176326 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI CALDERWOOD, STUART KEITH, SHERMAN, MICHAEL Y · 2014 to 2018
$1.8M
Gene Repression by HSF1 during hyperthermia and stressesR01CA094397 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI CALDERWOOD, STUART KEITH · 2002 to 2006
$1.5M
NCI NIH HHS R01 CA047407NCI NIH HHS R0-1CA047407NCI NIH HHS R01 CA094397NCI NIH HHS R0-1CA094397NCI NIH HHS R01 CA119045NCI NIH HHS R01CA119045NCI NIH HHS R01 CA176326
6 · The paper itself

Abstract

There is now compelling evidence to indicate a place for heat shock factor 1 (HSF1) in mammary carcinogenesis, tumour progression and metastasis. Here we have investigated a role for HSF1 in regulating the expression of the stem cell renewal factor β-catenin in immortalized human mammary epithelial and carcinoma cells. We found HSF1 to be involved in regulating the translation of β-catenin, by investigating effects of gain and loss of HSF1 on this protein. Interestingly, although HSF1 is a potent transcription factor, it was not directly involved in regulating levels of β-catenin mRNA. Instead, our data suggest a complex role in translational regulation. HSF1 was shown to regulate levels of the RNA-binding protein HuR that controlled β-catenin translation. An extra complexity was added to this scenario when it was shown that the long non-coding RNA molecule lincRNA-p21, known to be involved in β-catenin mRNA (CTNNB1) translational regulation, was controlled by HSF1 repression. We have shown previously that HSF1 was positively regulated through phosphorylation by mammalian target of rapamycin (mTOR) kinase on a key residue, serine 326, essential for transcriptional activity. In this study, we found that mTOR knockdown not only decreased HSF1-S326 phosphorylation in mammary cells, but also decreased β-catenin expression through a mechanism requiring HuR. Our data point to a complex role for HSF1 in the regulation of HuR and β-catenin expression that may be significant in mammary carcinogenesis.

Indexed as

Gene Expression Regulation, Neoplasticbeta CateninBreast NeoplasmsCell Line, TumorDNA-Binding ProteinsELAV-Like Protein 1ELAV ProteinsFemaleHeat Shock Transcription FactorsHumansNeoplasm ProteinsRNA, Long NoncodingTOR Serine-Threonine KinasesTranscription Factorsbeta CateninCTNNB1 protein, humanDNA-Binding ProteinsELAVL1 protein, humanELAV-Like Protein 1ELAV ProteinsHeat Shock Transcription FactorsHSF1 protein, humanMTOR protein, humanNeoplasm ProteinsRNA, Long NoncodingTOR Serine-Threonine KinasesTranscription Factors

Identifiers

PMID24954509
PMCPMC4275421
OpenAlexW2081787112

What OpenQuestion holds

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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.