Evidence map›Paper›PMID 26771843›Full record

ArticleOncotarget2016

Decreased expression of B7-H3 reduces the glycolytic capacity and sensitizes breast cancer cells to AKT/mTOR inhibitors.

Caroline E Nunes-Xavier, Karine Flem Karlsen, Christina Tekle, Cathrine Pedersen, Tove Øyjord, Vesa Hongisto, Jahn M Nesland, Ming Tan, Kristine Kleivi Sahlberg, Øystein Fodstad

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
3.9field-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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.

  1. Pooled it
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  14. B7-H3 suppresses CD8Journal of Cancer · 2024
    Article
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  18. Integrated Bioinformatics Analysis Revealed Immune Checkpoint Genes Relevant to Type 2 Diabetes.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024
    Article
  19. Targeting glycolytic pathway in fibroblast-like synoviocytes for rheumatoid arthritis therapy: challenges and opportunities.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Review
  20. Article
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

10 authors at 3 institutions in 2 countries.

Caroline E Nunes-XavierDepartment of Tumor Biology, Institute for Cancer Research, Oslo University Hospital Radiumhospitalet, Oslo, Norway.
Karine Flem KarlsenDepartment of Tumor Biology, Institute for Cancer Research, Oslo University Hospital Radiumhospitalet, Oslo, Norway.
Christina TekleDepartment of Tumor Biology, Institute for Cancer Research, Oslo University Hospital Radiumhospitalet, Oslo, Norway.
Cathrine PedersenDepartment of Genetics, Institute for Cancer Research, Oslo University Hospital Radiumhospitalet, Oslo, Norway.
Tove ØyjordDepartment of Tumor Biology, Institute for Cancer Research, Oslo University Hospital Radiumhospitalet, Oslo, Norway.
Vesa HongistoMisvik Biology Oy, Turku, Finland.
Jahn M NeslandDepartment of Pathology, Oslo University Hospital Radiumhospitalet, Oslo, Norway.
Ming TanDepartment of Oncologic Sciences, Mitchell Cancer Institute, University of South Alabama, Mobile, AL, USA.
Kristine Kleivi SahlbergDepartment of Research, Vestre Viken, Drammen, Norway.
Øystein FodstadDepartment of Tumor Biology, Institute for Cancer Research, Oslo University Hospital Radiumhospitalet, Oslo, Norway.
Oslo University Hospital · NOUniversity of South Alabama · USVestre Viken Hospital Trust · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

B7 family proteins are important immune response regulators, and can mediate oncogenic signaling and cancer development. We have used human triple-negative breast cancer cell lines with different expression levels of B7-H3 to evaluate its effects on the sensitivity to 22 different anticancer compounds in a drug screen. API-2 (triciribidine) and everolimus (RAD-001), two inhibitors that target the PI3K/AKT/mTOR pathway, showed enhanced inhibition of cell viability and proliferation in B7-H3 knockdown tumor cells compared to their B7-H3 expressing counterparts. Similar inhibition was seen in control cells treated with an anti-B7-H3 monoclonal antibody. In B7-H3 overexpressing cells, the effects of the two drugs were reduced, supported also by in vivo experiments in which B7-H3 overexpressing xenografts were less sensitive to everolimus than control tumors. In API-2 and everolimus-treated B7-H3 overexpressing cells, phospho-mTOR levels were decreased. However, phosphorylation of p70S6K was differentially regulated in B7-H3 cells treated with API-2 or everolimus, suggesting a different B7-H3-mediated mechanism downstream of mTOR. Both API-2 and everolimus decreased the glycolysis of the cells, whereas knockdown of B7-H3 decreased and B7-H3 overexpression increased the glycolytic capacity. In conclusion, we have unveiled a previously unknown relationship between B7-H3 expression and glycolytic capacity in tumor cells, and found that B7-H3 confers resistance to API-2 and everolimus. The results provide novel insights into the function of B7-H3 in cancer, and suggest that targeting of B7-H3 may be a novel alternative to improve current anticancer therapies.

Indexed as

AnimalsB7 AntigensCell Line, TumorFemaleGlycolysisHumansMiceMice, Inbred BALB CMice, NudePhosphorylationProtein Kinase InhibitorsProto-Oncogene Proteins c-aktSignal TransductionTOR Serine-Threonine KinasesTriple Negative Breast NeoplasmsB7 AntigensCD276 protein, humanMTOR protein, humanProtein Kinase InhibitorsProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesAPI-2breast cancer cellsCD276/B7-H3everolimusglycolysis

Identifiers

PMID26771843
PMCPMC4872756
OpenAlexW2260118114

What OpenQuestion holds

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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.