Evidence map›Paper›PMID 26318292›Full record

ArticleOncotarget2015

Metabolic alterations caused by HNF1β expression in ovarian clear cell carcinoma contribute to cell survival.

Yasuaki Amano, Masaki Mandai, Ken Yamaguchi, Noriomi Matsumura, Budiman Kharma, Tsukasa Baba, Kaoru Abiko, Junzo Hamanishi, Yumiko Yoshioka, Ikuo Konishi

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 16% 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

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

  1. Clinical practice guidelines for endometriosis in Japan (The 3rd edition).The journal of obstetrics and gynaecology research · 2022
    Guideline
  2. Review
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  12. Metabolic reprogramming in epithelial ovarian cancer.American journal of translational research · 2021
    Review
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  15. Article
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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

10 authors at 2 institutions in 1 country.

Yasuaki AmanoDepartment of Gynecology and Obstetrics, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Masaki MandaiDepartment of Gynecology and Obstetrics, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Ken YamaguchiDepartment of Gynecology and Obstetrics, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Noriomi MatsumuraDepartment of Gynecology and Obstetrics, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Budiman KharmaDepartment of Gynecology and Obstetrics, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Tsukasa BabaDepartment of Gynecology and Obstetrics, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Kaoru AbikoDepartment of Gynecology and Obstetrics, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Junzo HamanishiDepartment of Gynecology and Obstetrics, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Yumiko YoshiokaDepartment of Gynecology and Obstetrics, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Ikuo KonishiDepartment of Gynecology and Obstetrics, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Kyoto University · JPKindai University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HNF1β is expressed exclusively in ovarian clear cell carcinoma (OCCC) and not in other ovarian cancers, regarded as a hallmark of this tumor. This implies its central role in the unique character of OCCC, including resistance to chemotherapy, but its exact role and influence in cancer biology or the molecular bases of its function are largely unknown. Using comprehensive metabolome analysis of HNF1β_shRNA-stable cell lines, we show here that HNF1β drastically alters intracellular metabolism, especially in direction to enhance aerobic glycolysis, so called the "Warburg effect". The consequence of the metabolic change contributed cell survival under stresses such as hypoxia and chemo-reagent, only when sufficient glucose supply was available. Augmented cell survival was based on the reduced ROS activity derived from metabolic alteration such as shift from oxidative phosphorylation to glycolysis and increased intracellular anti-oxidant, glutathione (GSH). One of the cystine transporters, rBAT is likely to play a major role in this GSH increase. These data suggest that HNF1β, possibly induced by stressful microenvironment in the endometriotic cyst, confers survival advantage to the epithelial cells, which leads to the occurrence of OCCC, a chemo-resistant phenotype of ovarian cancer.

Indexed as

MetabolomeAdenocarcinoma, Clear CellAmino Acid Transport Systems, BasicAmino Acid Transport Systems, NeutralAntineoplastic AgentsBlotting, WesternCell HypoxiaCell Line, TumorCell ProliferationCell SurvivalCisplatinDrug Resistance, NeoplasmFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticGlutathioneAmino Acid Transport Systems, BasicAmino Acid Transport Systems, NeutralAntineoplastic AgentsCisplatinGlutathioneGlutathione DisulfideHepatocyte Nuclear Factor 1-betaReactive Oxygen SpeciesSLC3A1 protein, humanaerobic glycolysisHNF1βmetabolome analysisovarian clear cell carcinomaROS

Identifiers

PMID26318292
PMCPMC4694881
OpenAlexW1829991870

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.