Evidence map›Paper›PMID 23576571›Full record

ArticleMolecular cancer research : MCR2013

CYP1A1 regulates breast cancer proliferation and survival.

Mariangellys Rodriguez, David A Potter

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
3.0field-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

57 citing papers in PubMed, 118 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

2 authors at 1 institution in 1 country.

Mariangellys RodriguezDivision of Hematology, Oncology and Transplantation, Department of Medicine, The Masonic Cancer Center, University of Minnesota, Minneapolis, Minnesota 55455, USA.
David A Potter
University of Minnesota · US

Funding

Women's CancerP30CA077598 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI Douglas Yee · 1998 to 2026
$100.4M
TRAINING GRANT IN MICROBIOLOGY/CANCER RESEARCHT32CA009138 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI Scott M. Dehm · 1985 to 2026
$11.3M
Epoxygenease Mechanisms of Breast Cancer ProgressionR01CA113570 · NCI · UNIVERSITY OF MINNESOTA · PI POTTER, DAVID ALEXANDER · 2005 to 2008
$918k
Role of IGF-1R in breast cancer proliferation and survival via CYP1A1 epoxygenaseF31CA144084 · NCI · UNIVERSITY OF MINNESOTA · PI RODRIGUEZ, MARIANGELLYS · 2009 to 2012
$106k
NCI NIH HHS F31CA144084-02NCI NIH HHS P30CA077598NCI NIH HHS R01 CA113570NCI NIH HHS R01CA113570NCI NIH HHS T32 CA009138NCI NIH HHS T32 CA009138-38
6 · The paper itself

Abstract

Cytochrome P450-1A1 (CYP1A1) is an extrahepatic phase I metabolizing enzyme whose expression is suppressed under physiologic conditions but can be induced by substrates via the aryl hydrocarbon receptor (AhR). Recent studies have shown that the majority of breast cancer tumors constitutively express CYP1A1. These findings led us to test the hypothesis that CYP1A1 promotes breast cancer progression by evaluating the effects of CYP1A1 knockdown on the proliferation and survival of the MCF7 and MDA-MB-231 lines. Independently of estrogen receptor status, CYP1A1 knockdown decreased colony formation, decreased cell proliferation, blocked the cell cycle at G0-G1 associated with reduction of cyclin D1, and increased apoptosis associated with reduction of survivin. CYP1A1 knockdown markedly increased phosphorylation of AMP-activated protein kinase (AMPK) and decreased phosphorylation of AKT, extracellular signal-regulated kinases 1 and 2 (ERK1/2), and 70-kDa ribosomal protein S6 kinase (P70S6K). AMPK inhibition by compound C partially abrogated the proapoptotic effects of CYP1A1 knockdown, suggesting that effects of CYP1A1 knockdown are mediated in part through AMPK signaling. Consistent with CYP1A1 knockdown, pharmacologic reduction of CYP1A1 levels by the phytopolyphenol carnosol also correlated with impaired proliferation and induced AMPK phosphorylation. These results indicate that reduction of basal CYP1A1 expression is critical for inhibition of proliferation, which is not affected by α-naphthoflavone-mediated inhibition of CYP1A1 activity nor modulated by AhR silencing. This study supports the notion that CYP1A1 promotes breast cancer proliferation and survival, at least in part, through suppression of AMPK signaling and that reduction of CYP1A1 levels is a potential strategy for breast cancer therapeutics.

Indexed as

AbietanesAMP-Activated Protein KinasesBreast NeoplasmsCell CycleCell DeathCell Line, TumorCell ProliferationCell SurvivalCytochrome P-450 CYP1A1Enzyme ActivationExtracellular Signal-Regulated MAP KinasesFemaleGene Knockdown TechniquesHumansModels, BiologicalProto-Oncogene Proteins c-aktAbietanesAMP-Activated Protein KinasescarnosolCytochrome P-450 CYP1A1Extracellular Signal-Regulated MAP KinasesProto-Oncogene Proteins c-aktReceptors, Aryl HydrocarbonRNA, Small Interfering

Identifiers

PMID23576571
PMCPMC3720830
OpenAlexW2124851572

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.