Evidence map›Paper›PMID 21924251›Full record

ArticleBiochemical pharmacology2011

Generation of stable reporter breast cancer cell lines for the identification of ER subtype selective ligands.

Erin K Shanle, John R Hawse, Wei Xu

Abstract read
In one paragraph

Article in Biochemical pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

12 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Antiestrogens in combination with immune checkpoint inhibitors in breast cancer immunotherapy.The Journal of steroid biochemistry and molecular biology · 2019
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Differential action of monohydroxylated polycyclic aromatic hydrocarbons with estrogen receptors α and β.Toxicological sciences : an official journal of the Society of Toxicology · 2013
    Article
  12. Article
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

3 authors at 2 institutions in 1 country.

Erin K ShanleMcArdle Laboratory for Cancer Research, University of Wisconsin, Madison, WI 53706, USA.
John R Hawse
Wei Xu
University of Wisconsin–Madison · USMayo Clinic in Arizona · US

Funding

Molecular & Environmental Toxicology Pre-& Postdoctoral Training ProgramT32ES007015 · NIEHS · UNIVERSITY OF WISCONSIN-MADISON · PI CHRISTOPHER A BRADFIELD · 1985 to 2026
$11.5M
Transcriptional Regulation of Estrogen Receptor (ER) by CARM1R01CA125387 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI XU, WEI · 2008 to 2012
$1.6M
Identification of ERalpha/ERbeta Heterodimer-specific Ligands by HTSR03MH089442 · NIMH · UNIVERSITY OF WISCONSIN-MADISON · PI XU, WEI · 2009 to 2010
$74k
NCI NIH HHS R01 CA125387NCI NIH HHS R01CA125387NIEHS NIH HHS T32 ES007015NIMH NIH HHS R03 MH089442NIMH NIH HHS R03MH089442
6 · The paper itself

Abstract

Estrogen signaling is mediated by two estrogen receptors (ERs), ERα and ERβ, which have unique roles in the regulation of breast cancer cell proliferation. ERα induces proliferation in response to estrogen and ERβ inhibits proliferation in breast cancer cells, suggesting that ERβ selective ligands may be beneficial for promoting the anti-proliferative action of ERβ. Subtype selective ligands can be identified using transcriptional assays, but cell lines in which ERα or ERβ are independently expressed are required. Of the available reporter cell lines, none have been generated in breast cancer cells to identify subtype selective ligands. Here we describe the generation of two isogenic breast cancer cell lines, Hs578T-ERαLuc and Hs578T-ERβLuc, with stable integration of an estrogen responsive luciferase reporter gene. Hs578T-ERαLuc and Hs578T-ERβLuc cell lines are highly sensitive to estrogenic chemicals and ER subtype selective ligands, providing a tool to characterize the transcriptional potency and subtype selectivity of estrogenic ligands in the context of breast cancer cells. In addition to measuring reporter activity, ERβ target gene expression and growth inhibitory effects of ERβ selective ligands can be determined as biological endpoints. The finding that activation of ERβ by estrogen or ERβ selective natural phytoestrogens inhibits the growth of Hs578T-ERβ cells implies therapeutic potential for ERβ selective ligands in breast cancer cells that express ERβ.

Indexed as

Antineoplastic AgentsApigeninBreast NeoplasmsCell Line, TumorDoxorubicinEstrogen Receptor alphaEstrogen Receptor betaFemaleFlavanonesGene Expression Regulation, NeoplasticGenes, ReporterHumansLigandsLuciferasesAntineoplastic AgentsApigeninapigetrinDoxorubicinEstrogen Receptor alphaEstrogen Receptor betaFlavanonesLigandsliquiritigeninLuciferases

Identifiers

PMID21924251
PMCPMC3210412
OpenAlexW2093485170

What OpenQuestion holds

Textmetadata
LicenceTDM
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.