PMID- 10944171
OWN - NLM
STAT- MEDLINE
DCOM- 20001107
LR  - 20240414
IS  - 0022-3751 (Print)
IS  - 1469-7793 (Electronic)
IS  - 0022-3751 (Linking)
VI  - 527 Pt 1
IP  - Pt 1
DP  - 2000 Aug 15
TI  - Store depletion and store-operated Ca2+ current in human prostate cancer LNCaP 
      cells: involvement in apoptosis.
PG  - 71-83
AB  - 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.
FAU - Skryma, R
AU  - Skryma R
AD  - Laboratoire de Physiologie Cellulaire, INSERM EPI-9938, Villeneuve d'Ascq, 
      France.
FAU - Mariot, P
AU  - Mariot P
FAU - Bourhis, X L
AU  - Bourhis XL
FAU - Coppenolle, F V
AU  - Coppenolle FV
FAU - Shuba, Y
AU  - Shuba Y
FAU - Vanden Abeele, F
AU  - Vanden Abeele F
FAU - Legrand, G
AU  - Legrand G
FAU - Humez, S
AU  - Humez S
FAU - Boilly, B
AU  - Boilly B
FAU - Prevarskaya, N
AU  - Prevarskaya N
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Physiol
JT  - The Journal of physiology
JID - 0266262
RN  - 0 (Androgens)
RN  - 0 (Calcium Channels)
RN  - 67526-95-8 (Thapsigargin)
RN  - 6I3K30563S (Lanthanum)
RN  - 7OV03QG267 (Nickel)
RN  - EC 7.2.2.10 (Calcium-Transporting ATPases)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Androgens/pharmacology
MH  - *Apoptosis
MH  - Calcium/metabolism/*physiology
MH  - Calcium Channels/drug effects/*metabolism
MH  - Calcium-Transporting ATPases/antagonists & inhibitors
MH  - Electric Conductivity
MH  - Humans
MH  - Lanthanum/pharmacology
MH  - Male
MH  - Microscopy, Fluorescence
MH  - Nickel/pharmacology
MH  - Patch-Clamp Techniques
MH  - Prostatic Neoplasms/metabolism/*physiopathology
MH  - Thapsigargin/pharmacology
MH  - Tumor Cells, Cultured
PMC - PMC2270062
EDAT- 2000/08/16 11:00
MHDA- 2001/02/28 10:01
PMCR- 2001/08/15
CRDT- 2000/08/16 11:00
PHST- 2000/08/16 11:00 [pubmed]
PHST- 2001/02/28 10:01 [medline]
PHST- 2000/08/16 11:00 [entrez]
PHST- 2001/08/15 00:00 [pmc-release]
AID - PHY_0641 [pii]
AID - 10.1111/j.1469-7793.2000.00071.x [doi]
PST - ppublish
SO  - J Physiol. 2000 Aug 15;527 Pt 1(Pt 1):71-83. doi: 
      10.1111/j.1469-7793.2000.00071.x.