Evidence map›Paper›PMID 10944171›Full record

ArticleThe Journal of physiology2000

Store depletion and store-operated Ca2+ current in human prostate cancer LNCaP cells: involvement in apoptosis.

R Skryma, P Mariot, X L Bourhis, F V Coppenolle, Y Shuba, F Vanden Abeele, G Legrand, S Humez, B Boilly, N Prevarskaya

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In one paragraph

Article in The Journal of physiology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.5field-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

37 citing papers in PubMed, 120 citations in OpenAlex.

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  14. Distinct Cellular Calcium Metabolism in Radiation-sensitive RKO Human Colorectal Cancer Cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2014
    Article
  15. TRPV6 calcium channel translocates to the plasma membrane via Orai1-mediated mechanism and controls cancer cell survival.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  16. Article
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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.

R SkrymaLaboratoire de Physiologie Cellulaire, INSERM EPI-9938, Villeneuve d'Ascq, France.
P Mariot
X L Bourhis
F V Coppenolle
Y Shuba
F Vanden Abeele
G Legrand
S Humez
B Boilly
N Prevarskaya
Inserm · FRLaboratoire de Physiologie CellulaireLaboratoire de Biologie du Développement · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. In the present study, we investigated the mechanisms involved in the induction of apoptosis by the Ca2+-ATPase inhibitor thapsigargin (TG), in androgen-sensitive human prostate cancer LNCaP cells. 2. Exposure of fura-2-loaded LNCaP cells to TG in the presence of extracellular calcium produced an increase in intracellular Ca2+, the first phase of which was associated with depletion of intracellular stores and the second one with consecutive extracellular Ca2+ entry through plasma membrane, store-operated Ca2+ channels (SOCs). 3. For the first time we have identified and characterized the SOC-mediated membrane current (Istore) in prostate cells using whole-cell, cell-attached, and perforated patch-clamp techniques, combined with fura-2 microspectrofluorimetric and Ca2+-imaging measurements. 4. Istore in LNCaP cells lacked voltage-dependent gating and displayed an inwardly rectifying current-voltage relationship. The unitary conductance of SOCs with 80 mM Ca2+ as a charge carrier was estimated at 3.2 +/- 0.4 pS. The channel has a high selectivity for Ca2+ over monovalent cations and is inhibited by Ni2+ (0.5-3 mM) and La3+ (1 microM). 5. Treatment of LNCaP cells with TG (0.1 microM) induced apoptosis as judged from morphological changes. Decreasing extracellular free Ca2+ to 200 nM or adding 0.5 mM Ni2+ enhanced TG-induced apoptosis. 6. The ability of TG to induce apoptosis was not reduced by loading the cells with intracellular Ca2+ chelator (BAPTA-AM). 7. These results indicate that in androgen-sensitive prostate cancer cells the depletion of intracellular Ca2+ stores may trigger apoptosis but that there is no requirement for the activation of store-activated Ca2+ current and sustained Ca2+ entry in induction and development of programmed cell death.

Indexed as

ApoptosisAndrogensCalciumCalcium ChannelsCalcium-Transporting ATPasesElectric ConductivityHumansLanthanumMaleMicroscopy, FluorescenceNickelPatch-Clamp TechniquesProstatic NeoplasmsThapsigarginTumor Cells, CulturedAndrogensCalciumCalcium ChannelsCalcium-Transporting ATPasesLanthanumNickelThapsigargin

Identifiers

PMID10944171
PMCPMC2270062
OpenAlexW2074993010

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.