Evidence map›Paper›PMID 25966904›Full record

ArticleJournal of molecular cell biology2015

Synergistic control of sex hormones by 17β-HSD type 7: a novel target for estrogen-dependent breast cancer.

Xiaoqiang Wang, Catherine Gérard, Jean-François Thériault, Donald Poirier, Charles J Doillon, Sheng-Xiang Lin

Open access · bronzeAbstract read
In one paragraph

Article in Journal of molecular cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

11 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  4. Targeting macrophagic 17Acta pharmaceutica Sinica. B · 2023
    Article
  5. The Obesity-Related Metabolic Gene HSD17B8 Protects Against Breast Cancer: High RNA/Protein Expression Means a Better Prognosis.Medical science monitor : international medical journal of experimental and clinical research · 2022
    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

6 authors at 2 institutions in 1 country.

Xiaoqiang WangLaboratory of Molecular Endocrinology and Oncology, Centre Hospitalier Universitaire de Québec Research Center (CHUL, CHU) and Laval University, Québec City, Québec, G1V4G2, Canada.
Catherine GérardLaboratory of Molecular Endocrinology and Oncology, Centre Hospitalier Universitaire de Québec Research Center (CHUL, CHU) and Laval University, Québec City, Québec, G1V4G2, Canada.
Jean-François ThériaultLaboratory of Molecular Endocrinology and Oncology, Centre Hospitalier Universitaire de Québec Research Center (CHUL, CHU) and Laval University, Québec City, Québec, G1V4G2, Canada.
Donald PoirierLaboratory of Molecular Endocrinology and Oncology, Centre Hospitalier Universitaire de Québec Research Center (CHUL, CHU) and Laval University, Québec City, Québec, G1V4G2, Canada.
Charles J DoillonLaboratory of Molecular Endocrinology and Oncology, Centre Hospitalier Universitaire de Québec Research Center (CHUL, CHU) and Laval University, Québec City, Québec, G1V4G2, Canada.
Sheng-Xiang LinLaboratory of Molecular Endocrinology and Oncology, Centre Hospitalier Universitaire de Québec Research Center (CHUL, CHU) and Laval University, Québec City, Québec, G1V4G2, Canada sxlin@crchul.ulaval.ca.
Centre hospitalier universitaire de Québec · CAUniversité Laval · CA

Funding

Canadian Institutes of Health Research MOP 89851Canadian Institutes of Health Research MOP 97917
6 · The paper itself

Abstract

17β-hydroxysteroid dehydrogenase (17β-HSD) type 1 is known as a critical target to block the final step of estrogen production in estrogen-dependent breast cancer. Recent confirmation of the role of dyhydroxytestosterone (DHT) in counteracting estrogen-induced cell growth prompted us to study the reductive 17β-HSD type 7 (17β-HSD7), which activates estrone while markedly inactivating DHT. The role of DHT in breast cancer cell proliferation is demonstrated by its independent suppression of cell growth in the presence of a physiological concentration of estradiol (E2). Moreover, an integral analysis of a large number of clinical samples in Oncomine datasets demonstrated the overexpression of 17β-HSD7 in breast carcinoma. Inhibition of 17β-HSD7 in breast cancer cells resulted in a lower level of E2 and a higher level of DHT, successively induced regulation of cyclinD1, p21, Bcl-2, and Bik, consequently arrested cell cycle in the G(0)/G(1) phase, and triggered apoptosis and auto-downregulation feedback of the enzyme. Such inhibition led to significant shrinkage of xenograft tumors with decreased cancer cell density and reduced 17β-HSD7 expression. Decreased plasma E2 and elevated plasma DHT levels were also found. Thus, the dual functional 17β-HSD7 is proposed as a novel target for estrogen-dependent breast cancer by regulating the balance of E2 and DHT. This demonstrates a conceptual advance on the general belief that the major role of this enzyme is in cholesterol metabolism.

Indexed as

17-Hydroxysteroid DehydrogenasesAndrogensApoptosisApoptosis Regulatory ProteinsBreast NeoplasmsCell Cycle CheckpointsCell ProliferationCholesterolCyclin D1Cyclin-Dependent Kinase Inhibitor p21DihydrotestosteroneEstradiolEstradiol DehydrogenasesEstrogensEstroneFemale17-Hydroxysteroid Dehydrogenases3 (or 17)-beta-hydroxysteroid dehydrogenaseAndrogensApoptosis Regulatory ProteinsBCL2 protein, humanBIK protein, humanCCND1 protein, humanCholesterolCyclin D1Cyclin-Dependent Kinase Inhibitor p21DihydrotestosteroneEstradiolEstradiol DehydrogenasesEstrogensEstroneHSD17B1 protein, humanMembrane ProteinsMitochondrial ProteinsMultifunctional EnzymesProto-Oncogene Proteins c-bcl-217β-hydroxysteroid dehydrogenase type 7breast cancersteroid enzyme inhibitionxenograft tumor

Identifiers

PMID25966904
PMCPMC4664117
OpenAlexW2193299443

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.