Evidence map›Paper›PMID 9343423›Full record

ArticleMolecular and cellular biology1997

Inhibition of trans-retinoic acid-resistant human breast cancer cell growth by retinoid X receptor-selective retinoids.

Q Wu, M I Dawson, Y Zheng, P D Hobbs, A Agadir, L Jong, Y Li, R Liu, B Lin, X K Zhang

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

27 citing papers in PubMed, 95 citations in OpenAlex.

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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

10 authors at 3 institutions in 1 country.

Q WuThe Burnham Institute, La Jolla Cancer Research Center, California 92037, USA.
M I Dawson
Y Zheng
P D Hobbs
A Agadir
L Jong
Y Li
R Liu
B Lin
X K Zhang
Sanford Burnham Prebys Medical Discovery Institute · USMenlo School · USSRI International · US

Funding

RETINOIC ACID RESPONSE IN HUMAN LUNG CANCERR01CA060988 · NCI · BURNHAM INSTITUTE FOR MEDICAL RESEARCH · PI ZHANG, XIAO-KUN · 1993 to 2002
$940k
NCI NIH HHS CA51933NCI NIH HHS CA60988
6 · The paper itself

Abstract

All-trans-retinoic acid (trans-RA) and other retinoids exert anticancer effects through two types of retinoid receptors, the RA receptors (RARs) and retinoid X receptors (RXRs). Previous studies demonstrated that the growth-inhibitory effects of trans-RA and related retinoids are impaired in certain estrogen-independent breast cancer cell lines due to their lower levels of RAR alpha and RARbeta. In this study, we evaluated several synthetic retinoids for their ability to induce growth inhibition and apoptosis in both trans-RA-sensitive and trans-RA-resistant breast cancer cell lines. Our results demonstrate that RXR-selective retinoids, particularly in combination with RAR-selective retinoids, could significantly induce RARbeta and inhibit the growth and induce the apoptosis of trans-RA-resistant, RAR alpha-deficient MDA-MB-231 cells but had low activity against trans-RA-sensitive ZR-75-1 cells that express high levels of RAR alpha. Using gel retardation and transient transfection assays, we found that the effects of RXR-selective retinoids on MDA-MB-231 cells were most likely mediated by RXR-nur77 heterodimers that bound to the RA response element in the RARbeta promoter and activated the RARbeta promoter in response to RXR-selective retinoids. In contrast, growth inhibition by RAR-selective retinoids in trans-RA-sensitive, RAR alpha-expressing cells most probably occurred through RXR-RAR alpha heterodimers that also bound to and activated the RARbeta promoter. In MDA-MB-231 clones stably expressing RAR alpha, both RARbeta induction and growth inhibition by RXR-selective retinoids were suppressed, while the effects of RAR-selective retinoids were enhanced. Together, our results demonstrate that activation of RXR can inhibit the growth of trans-RA-resistant MDA-MB-231 breast cancer cells and suggest that low cellular RAR alpha may regulate the signaling switch from RAR-mediated to RXR-mediated growth inhibition in breast cancer cells.

Indexed as

Antineoplastic AgentsApoptosisBinding, CompetitiveBreast NeoplasmsCell DivisionDNA-Binding ProteinsDrug ResistanceEvaluation Studies as TopicFemaleGene Expression Regulation, NeoplasticHumansIsomerismNuclear Receptor Subfamily 4, Group A, Member 1Receptors, Cytoplasmic and NuclearReceptors, Retinoic AcidReceptors, SteroidAntineoplastic AgentsDNA-Binding ProteinsNR4A1 protein, humanNuclear Receptor Subfamily 4, Group A, Member 1Receptors, Cytoplasmic and NuclearReceptors, Retinoic AcidReceptors, Steroidretinoic acid receptor betaRetinoidsRetinoid X ReceptorsTranscription FactorsTretinoin

Identifiers

PMID9343423
PMCPMC232513
OpenAlexW2096790906

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.