Evidence map›Paper›PMID 33619826›Full record

ArticleCancer science2021

Upregulation of glucocorticoid receptor-mediated glucose transporter 4 in enzalutamide-resistant prostate cancer.

Seiji Hoshi, Satoru Meguro, Hitomi Imai, Yuta Matsuoka, Yuki Yoshida, Akihumi Onagi, Ryo Tanji, Ruriko Honda-Takinami, Kanako Matsuoka, Tomoyuki Koguchi and 6 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Cancer science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

14 citing papers in PubMed, 15 citations in OpenAlex.

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  13. Correction.Cancer science · 2021
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 1 institution in 1 country.

Seiji HoshiDepartment of Urology, Fukushima Medical University School of Medicine, Fukushima, Japan.ORCID https://orcid.org/0000-0003-1545-1827
Satoru MeguroDepartment of Urology, Fukushima Medical University School of Medicine, Fukushima, Japan.
Hitomi ImaiDepartment of Urology, Fukushima Medical University School of Medicine, Fukushima, Japan.
Yuta MatsuokaDepartment of Urology, Fukushima Medical University School of Medicine, Fukushima, Japan.
Yuki YoshidaDepartment of Urology, Fukushima Medical University School of Medicine, Fukushima, Japan.
Akihumi OnagiDepartment of Urology, Fukushima Medical University School of Medicine, Fukushima, Japan.
Ryo TanjiDepartment of Urology, Fukushima Medical University School of Medicine, Fukushima, Japan.
Ruriko Honda-TakinamiDepartment of Urology, Fukushima Medical University School of Medicine, Fukushima, Japan.
Kanako MatsuokaDepartment of Urology, Fukushima Medical University School of Medicine, Fukushima, Japan.
Tomoyuki KoguchiDepartment of Urology, Fukushima Medical University School of Medicine, Fukushima, Japan.
Junya HataDepartment of Urology, Fukushima Medical University School of Medicine, Fukushima, Japan.
Yuichi SatoDepartment of Urology, Fukushima Medical University School of Medicine, Fukushima, Japan.
Hidenori AkaihataDepartment of Urology, Fukushima Medical University School of Medicine, Fukushima, Japan.
Masao KataokaDepartment of Urology, Fukushima Medical University School of Medicine, Fukushima, Japan.
Soichiro OgawaDepartment of Urology, Fukushima Medical University School of Medicine, Fukushima, Japan.
Yoshiyuki KojimaDepartment of Urology, Fukushima Medical University School of Medicine, Fukushima, Japan.
Fukushima Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Enzalutamide (Enz) is a second-generation androgen receptor (AR) antagonist for castration-resistant prostate cancer (CRPC) therapy, and it prolongs survival time in these patients. However, during Enz treatment, CRPC patients usually acquire resistance to Enz and often show cross-resistance to other AR signaling inhibitors. Although glucocorticoid receptor (GR) is involved in this resistance, the role of GR has not yet been clarified. Here, we report that chronic Enz treatment induced GR-mediated glucose transporter 4 (GLUT4) upregulation, and that upregulation was associated with resistance to Enz and other AR signaling inhibitors. Additionally, inhibition of GLUT4 suppressed cell proliferation in Enz-resistant prostate cancer cells, which recovered from Enz resistance and cross-resistance without changes in GR expression. Thus, a combination of Enz and a GLUT4 inhibitor could be useful in Enz-resistant CRPC patients.

Indexed as

Androgen Receptor AntagonistsAntineoplastic AgentsBenzamidesCell Line, TumorCell ProliferationDrug Resistance, NeoplasmGlucoseGlucose Transporter Type 1Glucose Transporter Type 3Glucose Transporter Type 4Glucose Transport Proteins, FacilitativeHumansMaleNitrilesPhenylthiohydantoinProstatic Neoplasms, Castration-ResistantAndrogen Receptor AntagonistsAntineoplastic AgentsBenzamidesenzalutamideGlucoseGlucose Transporter Type 1Glucose Transporter Type 3Glucose Transporter Type 4Glucose Transport Proteins, FacilitativeNitrilesPhenylthiohydantoinReceptors, AndrogenReceptors, GlucocorticoidSLC2A12 protein, humanSLC2A1 protein, humanSLC2A3 protein, humanSLC2A4 protein, humanandrogen receptorenzalutamideglucocorticoid receptorglucose transporter 4prostate cancer

Identifiers

PMID33619826
PMCPMC8088914
OpenAlexW3131178822

What OpenQuestion holds

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LicenceCC BY-NC
Read underepoch 390

Registered trials

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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.