Evidence map›Paper›PMID 27458161›Full record

ArticleOncotarget2017

Crosstalk between integrin αvβ3 and ERα contributes to thyroid hormone-induced proliferation of ovarian cancer cells.

Meng-Ti Hsieh, Le-Ming Wang, Chun A Changou, Yu-Tang Chin, Yu-Chen S H Yang, Hsuan-Yu Lai, Sheng-Yang Lee, Yung-Ning Yang, Jacqueline Whang-Peng, Leroy F Liu and 3 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.6field-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

26 citing papers in PubMed, 54 citations in OpenAlex.

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  10. The power of heteronemin in cancers.Journal of biomedical science · 2022
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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

13 authors at 3 institutions in 2 countries.

Meng-Ti HsiehTaipei Cancer Center, Taipei Medical University, Taipei, Taiwan.
Le-Ming WangDepartment of Obstetrics and Gynecology, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan.
Chun A ChangouThe PhD Program for Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan.
Yu-Tang ChinTaipei Cancer Center, Taipei Medical University, Taipei, Taiwan.
Yu-Chen S H YangJoint Biobank, Office of Human Research, Taipei Medical University, Taipei, Taiwan.
Hsuan-Yu LaiTaipei Cancer Center, Taipei Medical University, Taipei, Taiwan.
Sheng-Yang LeeDepartment of Dentistry, Wan-Fang Medical Center, Taipei Medical University, Taipei, Taiwan.
Yung-Ning YangDepartment of Pediatrics, E-DA Hospital, I-Shou University, Kaohsiung, Taiwan.
Jacqueline Whang-PengTaipei Cancer Center, Taipei Medical University, Taipei, Taiwan.
Leroy F LiuTaipei Cancer Center, Taipei Medical University, Taipei, Taiwan.
Hung-Yun LinTaipei Cancer Center, Taipei Medical University, Taipei, Taiwan.
Shaker A MousaPharmaceutical Research Institute, Albany College of Pharmacy and Health Sciences, Albany, New York, USA.
Paul J DavisPharmaceutical Research Institute, Albany College of Pharmacy and Health Sciences, Albany, New York, USA.
Taipei Medical University · TWAlbany College of Pharmacy and Health Sciences · USWan Fang Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ovarian cancer is the leading cause of death in gynecological diseases. Thyroid hormone promotes proliferation of ovarian cancer cells via cell surface receptor integrin αvβ3 that activates extracellular regulated kinase (ERK1/2). However, the mechanisms are still not fully understood. Thyroxine (T4) at a physiologic total hormone concentration (10-7 M) significantly increased proliferating cell nuclear antigen (PCNA) abundance in these cell lines, as did 3, 5, 3'-triiodo-L-thyronine (T3) at a supraphysiologic concentration. Thyroid hormone (T4 and T3) treatment of human ovarian cancer cells resulted in enhanced activation of the Ras/MAPK(ERK1/2) signal transduction pathway. An MEK inhibitor (PD98059) blocked hormone-induced cell proliferation but not ER phosphorylation. Knock-down of either integrin αv or β3 by RNAi blocked thyroid hormone-induced phosphorylation of ERK1/2. We also found that thyroid hormone causes elevated phosphorylation and nuclear enrichment of estrogen receptor α (ERα). Confocal microscopy indicated that both T4 and estradiol (E2) caused nuclear translocation of integrin αv and phosphorylation of ERα. The specific ERα antagonist (ICI 182,780; fulvestrant) blocked T4-induced ERK1/2 activation, ERα phosphorylation, PCNA expression and proliferation. The nuclear co-localization of integrin αv and phosphorylated ERα was inhibited by ICI. ICI time-course studies indicated that mechanisms involved in T4- and E2-induced nuclear co-localization of phosphorylated ERα and integrin αv are dissimilar. Chromatin immunoprecipitation results showed that T4-induced binding of integrin αv monomer to ERα promoter and this was reduced by ICI. In summary, thyroid hormone stimulates proliferation of ovarian cancer cells via crosstalk between integrin αv and ERα, mimicking functions of E2.

Indexed as

Signal TransductionCell Line, TumorCell ProliferationEstrogen Receptor alphaFemaleHumansIntegrin alphaVbeta3Mitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Ovarian NeoplasmsProtein BindingThyroid HormonesEstrogen Receptor alphaIntegrin alphaVbeta3Mitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Thyroid HormonesERα crosstalkintegrin αvβ3ovarian cancerthyroid hormone

Identifiers

PMID27458161
PMCPMC5421843
OpenAlexW2504986314

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.