Evidence map›Paper›PMID 27819670›Full record

ArticleOncogene2017

HSP110 promotes colorectal cancer growth through STAT3 activation.

K Berthenet, A'dem Bokhari, A Lagrange, G Marcion, C Boudesco, S Causse, A De Thonel, M Svrcek, A R Goloudina, S Dumont and 8 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 6% 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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 104 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

18 authors at 3 institutions in 1 country.

K BerthenetINSERM, UMR866, Université de Bourgogne Franche-Comté, Faculté des Sciences de Santé, Dijon, France.
A'dem BokhariINSERM, UMR 938, Equipe Labellisée par la Ligue Nationale Contre le Cancer, Paris, France.
A LagrangeINSERM, UMR 938, Equipe Labellisée par la Ligue Nationale Contre le Cancer, Paris, France.
G MarcionINSERM, UMR866, Université de Bourgogne Franche-Comté, Faculté des Sciences de Santé, Dijon, France.
C BoudescoINSERM, UMR866, Université de Bourgogne Franche-Comté, Faculté des Sciences de Santé, Dijon, France.
S CausseINSERM, UMR866, Université de Bourgogne Franche-Comté, Faculté des Sciences de Santé, Dijon, France.ORCID 0000-0003-3246-3491
A De ThonelCNRS, UMR7216 Epigenetics and Cell Fate, Paris, France.
M SvrcekINSERM, UMR 938, Equipe Labellisée par la Ligue Nationale Contre le Cancer, Paris, France.
A R GoloudinaINSERM, UMR866, Université de Bourgogne Franche-Comté, Faculté des Sciences de Santé, Dijon, France.
S DumontAP-HP, Hôpital St Antoine; Service d'Anatomie Pathologique, Paris, France.
A HammannINSERM, UMR866, Université de Bourgogne Franche-Comté, Faculté des Sciences de Santé, Dijon, France.
D S BiardCentre d'Etude Atomique, Paris, France.
O N DemidovINSERM, UMR866, Université de Bourgogne Franche-Comté, Faculté des Sciences de Santé, Dijon, France.
R SeigneuricINSERM, UMR866, Université de Bourgogne Franche-Comté, Faculté des Sciences de Santé, Dijon, France.
A DuvalINSERM, UMR 938, Equipe Labellisée par la Ligue Nationale Contre le Cancer, Paris, France.ORCID 0000-0003-1534-1724
A ColluraINSERM, UMR 938, Equipe Labellisée par la Ligue Nationale Contre le Cancer, Paris, France.
G JegoINSERM, UMR866, Université de Bourgogne Franche-Comté, Faculté des Sciences de Santé, Dijon, France.
C GarridoINSERM, UMR866, Université de Bourgogne Franche-Comté, Faculté des Sciences de Santé, Dijon, France.
Inserm · FRCentre National de la Recherche Scientifique · FRSorbonne Université · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heat shock protein 110 (HSP110) is induced by different stresses and, through its anti-apoptotic and chaperoning properties, helps cells survive these adverse situations. In colon cancers, HSP110 is abnormally abundant. We have recently shown that colorectal cancer patients with microsatellite instability (MSI) had an improved response to chemotherapy because they harbor an HSP110-inactivating mutation (HSP110DE9). In this work, we used patient biopsies, human colorectal cancer cells grown in vitro and in vivo (xenografts), and intestinal crypts to demonstrate that HSP110 is also involved in colon cancer growth. We showed that HSP110 induces colon cancer cell proliferation and that this effect is associated with STAT3 activation, specifically an increase in STAT3 phosphorylation, nuclear translocation and transcription factor activity. STAT3 inhibition blocks the proliferative effect of HSP110. From a molecular standpoint, we demonstrated that HSP110 directly binds to STAT3, thereby facilitating its phosphorylation by JAK2. Finally, we showed a correlation between HSP110 expression and STAT3 phosphorylation in colon cancer patient samples. Thus, the expression of HSP110 in colon cancer contributes to STAT3-dependent tumor growth and the frequent inactivating mutation of this chaperone is probably an important event underlying the improved prognosis in colon cancer displaying MSI.

Indexed as

AnimalsBiopsyCell Line, TumorCell ProliferationColorectal NeoplasmsFemaleHSP110 Heat-Shock ProteinsHumansIntestinal MucosaMiceMice, NudeNeoplasm TransplantationPhosphorylationProtein BindingSTAT3 Transcription FactorHSP110 Heat-Shock ProteinsHSPH1 protein, humanSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID27819670
OpenAlexW2551088026

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.