Evidence map›Paper›PMID 27450545›Full record

ArticleBioscience reports2016

TRPV6 modulates proliferation of human pancreatic neuroendocrine BON-1 tumour cells.

Marek Skrzypski, Paweł A Kołodziejski, Stefan Mergler, Noushafarin Khajavi, Krzysztof W Nowak, Mathias Z Strowski

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

10 citing papers in PubMed, 14 citations in OpenAlex.

  1. TRPV6-Mediated CaCancers · 2026
    Review
  2. Article
  3. Article
  4. Review
  5. Bidirectional Allosteric Coupling between PIPInternational journal of molecular sciences · 2024
    Article
  6. Article
  7. Review
  8. Review
  9. TRP Channels in Digestive Tract Cancers.International journal of molecular sciences · 2020
    Review
  10. 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

6 authors at 3 institutions in 2 countries.

Marek SkrzypskiDepartment of Animal Physiology and Biochemistry, Poznań University of Life Sciences, 60-637 Poznań, Poland.
Paweł A KołodziejskiDepartment of Animal Physiology and Biochemistry, Poznań University of Life Sciences, 60-637 Poznań, Poland Department of Hepatology and Gastroenterology and Interdisciplinary Centre of Metabolism: Endocrinology, Diabetes and Metabolism, Charité-University Medicine Berlin, 13353 Berlin, Germany.
Stefan MerglerDepartment of Ophthalmology, Charité-University Medicine Berlin, 13353 Berlin, Germany.
Noushafarin KhajaviInstitute for Experimental Pediatric Endocrinology, Charité-University Medicine Berlin, 13353 Berlin, Germany.
Krzysztof W NowakDepartment of Animal Physiology and Biochemistry, Poznań University of Life Sciences, 60-637 Poznań, Poland.
Mathias Z StrowskiDepartment of Hepatology and Gastroenterology and Interdisciplinary Centre of Metabolism: Endocrinology, Diabetes and Metabolism, Charité-University Medicine Berlin, 13353 Berlin, Germany Medical Clinic 1, Department of Gastroenterology, Elblandklinik, 01662 Meissen, Germany mathias.strowski@charite.de.
University of Life Sciences in Poznań · PLCharité - Universitätsmedizin Berlin · DEHelios Kliniken · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Highly Ca(2+) permeable receptor potential channel vanilloid type 6 (TRPV6) modulates a variety of biological functions including calcium-dependent cell growth and apoptosis. So far, the role of TRPV6 in controlling growth of pancreatic neuroendocrine tumour (NET) cells is unknown. In the present study, we characterize the expression of TRPV6 in pancreatic BON-1 and QGP-1 NET cells. Furthermore, we evaluate the impact of TRPV6 on intracellular calcium, the activity of nuclear factor of activated T-cells (NFAT) and proliferation of BON-1 cells. TRPV6 expression was assessed by real-time PCR and Western blot. TRPV6 mRNA expression and protein production were down-regulated by siRNA. Changes in intracellular calcium levels were detected by fluorescence calcium imaging (fura-2/AM). NFAT activity was studied by NFAT reporter assay; cell proliferation by bromodeoxyuridine (BrdU), MTT and propidium iodine staining. TRPV6 mRNA and protein are present in BON-1 and QGP-1 NET-cells. Down-regulation of TRPV6 attenuates BON-1 cell proliferation. TRPV6 down-regulation is associated with decreased Ca(2+) response pattern and reduced NFAT activity. In conclusion, TRPV6 is expressed in pancreatic NETs and modulates cell proliferation via Ca(2+)-dependent mechanism, which is accompanied by NFAT activation.

Indexed as

ApoptosisCalciumCalcium ChannelsCell Line, TumorCell ProliferationDown-RegulationHumansNeuroendocrine TumorsNFATC Transcription FactorsPancreatic NeoplasmsRNA, MessengerRNA, Small InterferingTRPV Cation ChannelsCalciumCalcium ChannelsNFATC Transcription FactorsRNA, MessengerRNA, Small InterferingTRPV6 protein, humanTRPV Cation ChannelsBON-1calciumneuroendocrine tumourproliferationQGP-1TRPV6

Identifiers

PMID27450545
PMCPMC4995500
OpenAlexW2499804889

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.