Evidence map›Paper›PMID 27183905›Full record

ArticleOncotarget2016

Functional cooperation between KCa3.1 and TRPC1 channels in human breast cancer: Role in cell proliferation and patient prognosis.

Malika Faouzi, Frederic Hague, Dirk Geerts, Anne-Sophie Ay, Marie Potier-Cartereau, Ahmed Ahidouch, Halima Ouadid-Ahidouch

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
4.1field-weighted citation impact, top 7% 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

43 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
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  7. Functional cooperation between IKCell proliferation · 2023
    Article
  8. Imaging of KChemMedChem · 2023
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  9. IKCell death & disease · 2022
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  11. CaInternational journal of molecular sciences · 2022
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  16. Intermediate conductance CaFrontiers in insect 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

7 authors at 2 institutions in 3 countries.

Malika FaouziUniversity of Picardie Jules Verne, UFR of Sciences, EA4667 Laboratory of Cell and Molecular Physiology, SFR CAP-SANTE (FED 4231), Amiens, France.
Frederic HagueUniversity of Picardie Jules Verne, UFR of Sciences, EA4667 Laboratory of Cell and Molecular Physiology, SFR CAP-SANTE (FED 4231), Amiens, France.
Dirk GeertsDepartment of Pediatric Oncology/Hematology, Erasmus University Medical Center, 3015 GE Rotterdam, The Netherlands.
Anne-Sophie AyUniversity of Picardie Jules Verne, UFR of Sciences, EA4667 Laboratory of Cell and Molecular Physiology, SFR CAP-SANTE (FED 4231), Amiens, France.
Marie Potier-CartereauUniversity of Picardie Jules Verne, UFR of Sciences, EA4667 Laboratory of Cell and Molecular Physiology, SFR CAP-SANTE (FED 4231), Amiens, France.
Ahmed AhidouchUniversity of Picardie Jules Verne, UFR of Sciences, EA4667 Laboratory of Cell and Molecular Physiology, SFR CAP-SANTE (FED 4231), Amiens, France.
Halima Ouadid-AhidouchUniversity of Picardie Jules Verne, UFR of Sciences, EA4667 Laboratory of Cell and Molecular Physiology, SFR CAP-SANTE (FED 4231), Amiens, France.
Université de Picardie Jules Verne · FRQueen's Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intracellular Ca2+ levels are important regulators of cell cycle and proliferation. We, and others, have previously reported the role of KCa3.1 (KCNN4) channels in regulating the membrane potential and the Ca2+ entry in association with cell proliferation. However, the relevance of KC3.1 channels in cancer prognosis as well as the molecular mechanism of Ca2+ entry triggered by their activation remain undetermined. Here, we show that RNAi-mediated knockdown of KCa3.1 and/or TRPC1 leads to a significant decrease in cell proliferation due to cell cycle arrest in the G1 phase. These results are consistent with the observed upregulation of both channels in synchronized cells at the end of G1 phase. Additionally, knockdown of TRPC1 suppressed the Ca2+ entry induced by 1-EBIO-mediated KCa3.1 activation, suggesting a functional cooperation between TRPC1 and KCa3.1 in the regulation of Ca2+ entry, possibly within lipid raft microdomains where these two channels seem to co-localize. We also show significant correlations between KCa3.1 mRNA expression and poor patient prognosis and unfavorable clinical breast cancer parameters by mining large datasets in the public domain. Together, these results highlight the importance of KCa3.1 in regulating the proliferative mechanisms in breast cancer cells as well as in providing a promising novel target in prognosis and therapy.

Indexed as

Breast NeoplasmsCalciumCell ProliferationFemaleG1 Phase Cell Cycle CheckpointsGene Expression ProfilingGene Expression Regulation, NeoplasticHumansIntermediate-Conductance Calcium-Activated Potassium ChannelsKaplan-Meier EstimateMCF-7 CellsPrognosisRNA InterferenceTRPC Cation ChannelsCalciumIntermediate-Conductance Calcium-Activated Potassium ChannelsKCNN4 protein, humantransient receptor potential cation channel, subfamily C, member 1TRPC Cation Channelsbreast cancercalciumcell proliferationKCa3.1TRPC1

Identifiers

PMID27183905
PMCPMC5095010
OpenAlexW2416881184

What OpenQuestion holds

Textmetadata
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.