Evidence map›Paper›PMID 23431153›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

Calcium-activated chloride channel ANO1 promotes breast cancer progression by activating EGFR and CAMK signaling.

Adrian Britschgi, Anke Bill, Heike Brinkhaus, Christopher Rothwell, Ieuan Clay, Stephan Duss, Michael Rebhan, Pichai Raman, Chantale T Guy, Kristie Wetzel and 12 more

Open access · hybridAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 206 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
206citing papers in PubMed, 2 pooled it
11.4field-weighted citation impact, top 1% 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

206 citing papers in PubMed, 2 syntheses or guidelines pooled it, 319 citations in OpenAlex.

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  12. Organelle contact sites in cancer cells.Cell death & disease · 2026
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146 more citing papers are in PubMed but not listed here.

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

22 authors at 5 institutions in 3 countries.

Adrian BritschgiFriedrich Miescher Institute for Biomedical Research, CH-4058 Basel, Switzerland.
Anke Bill
Heike Brinkhaus
Christopher Rothwell
Ieuan Clay
Stephan Duss
Michael Rebhan
Pichai Raman
Chantale T Guy
Kristie Wetzel
Elizabeth George
M Oana Popa
Sarah Lilley
Hedaythul Choudhury
Martin Gosling
Louis Wang
Stephanie Fitzgerald
Jason Borawski
Jonathan Baffoe
Mark Labow
L Alex Gaither
Mohamed Bentires-Alj
Novartis (Switzerland) · CHPathways Behavioral Services · USFriedrich Miescher Institute · CHNovartis Institutes for BioMedical ResearchNovartis (United Kingdom) · GB

Funding

European Research Council 243211
6 · The paper itself

Abstract

The calcium-activated chloride channel anoctamin 1 (ANO1) is located within the 11q13 amplicon, one of the most frequently amplified chromosomal regions in human cancer, but its functional role in tumorigenesis has remained unclear. The 11q13 region is amplified in ∼15% of breast cancers. Whether ANO1 is amplified in breast tumors, the extent to which gene amplification contributes to ANO1 overexpression, and whether overexpression of ANO1 is important for tumor maintenance have remained unknown. We have found that ANO1 is amplified and highly expressed in breast cancer cell lines and primary tumors. Amplification of ANO1 correlated with disease grade and poor prognosis. Knockdown of ANO1 in ANO1-amplified breast cancer cell lines and other cancers bearing 11q13 amplification inhibited proliferation, induced apoptosis, and reduced tumor growth in established cancer xenografts. Moreover, ANO1 chloride channel activity was important for cell viability. Mechanistically, ANO1 knockdown or pharmacological inhibition of its chloride-channel activity reduced EGF receptor (EGFR) and calmodulin-dependent protein kinase II (CAMKII) signaling, which subsequently attenuated AKT, v-src sarcoma viral oncogene homolog (SRC), and extracellular signal-regulated kinase (ERK) activation in vitro and in vivo. Our results highlight the involvement of the ANO1 chloride channel in tumor progression and provide insights into oncogenic signaling in human cancers with 11q13 amplification, thereby establishing ANO1 as a promising target for therapy in these highly prevalent tumor types.

Indexed as

Gene AmplificationAnimalsAnoctamin-1ApoptosisBreast NeoplasmsCalcium-Calmodulin-Dependent Protein Kinase Type 2Cell Line, TumorCell SurvivalChloride ChannelsChromosomes, Human, Pair 11Enzyme ActivationErbB ReceptorsFemaleGene Knockdown TechniquesHumansMiceANO1 protein, humanAnoctamin-1Calcium-Calmodulin-Dependent Protein Kinase Type 2Chloride ChannelsEGFR protein, humanErbB ReceptorsNeoplasm Proteins

Identifiers

PMID23431153
PMCPMC3600458
OpenAlexW1996708800

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.