Evidence map›Paper›PMID 19775474›Full record

ArticleReproductive biology and endocrinology : RB&E2009

A novel variant of ER-alpha, ER-alpha36 mediates testosterone-stimulated ERK and Akt activation in endometrial cancer Hec1A cells.

Sheng-Li Lin, Li-Ying Yan, Xing-Wei Liang, Zhen-Bo Wang, Zhao-Yi Wang, Jie Qiao, Heide Schatten, Qing-Yuan Sun

Open access · goldAbstract read
In one paragraph

Article in Reproductive biology and endocrinology : RB&E, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 61 citations in OpenAlex.

  1. The role of ERK-1 and ERK-2 gene polymorphisms in PCOS pathogenesis.Reproductive biology and endocrinology : RB&E · 2022
    Article
  2. Article
  3. Review
  4. Article
  5. Estrogen Receptors and Estrogen-Induced Uterine Vasodilation in Pregnancy.International journal of molecular sciences · 2020
    Review
  6. The Role of ERα36 in Development and Tumor Malignancy.International journal of molecular sciences · 2020
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Role of ER-α36 in breast cancer by typical xenoestrogens.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Review
  16. Review
  17. Observational
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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

8 authors at 6 institutions in 2 countries.

Sheng-Li LinState Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China. linsl@ioz.ac.cn
Li-Ying Yan
Xing-Wei Liang
Zhen-Bo Wang
Zhao-Yi Wang
Jie Qiao
Heide Schatten
Qing-Yuan Sun
Chinese Academy of Sciences · CNCHI Health Creighton University Medical Center - Bergan Mercy · USInstitute of Zoology · CNPeking University · CNPeking University Third Hospital · CNUniversity of Missouri · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEndometrial cancer is one of the most common gynecologic malignancies and its incidence has recently increased. Experimental and epidemiological data support that testosterone plays an important role in the pathogenesis of endometrial cancer, but the underlying mechanism has not been fully understood. Recently, we identified and cloned a variant of estrogen receptor (ER) alpha, ER-alpha36. The aim of the present study was to investigate the role of ER-alpha36 in testosterone carcinogenesis.

methodsThe cellular localization of ER-alpha36 was determined by immunofluorescence. Hec1A endometrial cancer cells (Hec1A/V) and Hec1A cells with siRNA knockdown of ER-alpha36 (Hec1A/RNAi) were treated with testosterone, ERK and Akt phosphorylation was assessed by Western blot analysis. Furthermore, the kinase inhibitors U0126 and LY294002 and the aromatase inhibitor letrozole were used to elucidate the pathway underlying testosterone-induced activities.

resultsImmunofluorescence shows that ER-alpha36 was localized on the plasma membrane of the both ER-alpha- and androgen receptor-negative endometrial cancer Hec1A cells. Testosterone induced ERK and Akt phosphorylation, which could be abrogated by ER-alpha 36 shRNA knockdown or the kinase inhibitors, U0126 and LY294002, and the aromatase inhibitor letrozole.

conclusionTestosterone induces ERK and Akt phosphorylation via the membrane-initiated signaling pathways mediated by ER-alpha36, suggesting a possible involvement of ER-alpha 36 in testosterone carcinogenesis.

Indexed as

Aromatase InhibitorsCarcinomaCell MembraneEndometrial NeoplasmsEnzyme ActivationEstrogen Receptor alphaExtracellular Signal-Regulated MAP KinasesFemaleHumansLetrozoleNitrilesPhosphorylationProtein IsoformsProto-Oncogene Proteins c-aktSignal TransductionTestosteroneAromatase InhibitorsESR1 protein, humanEstrogen Receptor alphaExtracellular Signal-Regulated MAP KinasesLetrozoleNitrilesProtein IsoformsProto-Oncogene Proteins c-aktTestosteroneTriazoles

Identifiers

PMID19775474
PMCPMC2761922
OpenAlexW2097808175

What OpenQuestion holds

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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.