PMID- 12767895
OWN - NLM
STAT- MEDLINE
DCOM- 20040304
LR  - 20190922
IS  - 0143-4160 (Print)
IS  - 0143-4160 (Linking)
VI  - 34
IP  - 1
DP  - 2003 Jul
TI  - Mechanisms of ATP-induced calcium signaling and growth arrest in human prostate 
      cancer cells.
PG  - 75-85
AB  - This study investigates the calcium mechanisms involved in growth arrest induced 
      by extracellular ATP in DU-145 androgen-independent human prostate cancer cells. 
      Exposure of DU-145 cells to 100 microM ATP produced an increase in cytoplasmic 
      calcium concentration ([Ca(2+)](i)), due to a mobilization of calcium from the 
      endoplasmic reticulum stores and to subsequent capacitative calcium entry (CCE). 
      We have shown that this [Ca(2+)](i) increase occurs after stimulation by ATP of 
      the phospholipase C (PLC) pathway. For the first time, we have identified the 
      inositol 1,4,5-trisphosphate receptor (IP(3)R) isoforms expressed in this cell 
      line and have demonstrated a participation of protein kinase C in CCE. Using 
      fluorescence imaging, we have shown that a long-term treatment with ATP leads to 
      a decrease in the intraluminal endoplasmic reticulum calcium concentration as 
      well as in the amount of releasable Ca(2+). Modulating extracellular free calcium 
      concentrations indicated that variations in [Ca(2+)](i) did not affect the 
      ATP-induced growth arrest of DU-145 cells. However, treating cells with 1 nM 
      thapsigargin (TG) to deplete intracellular calcium pools prevented the growth 
      arrest induced by ATP. Altogether, these results indicate that growth arrest 
      induced in DU-145 cells by extracellular ATP is not correlated with an increase 
      in [Ca(2+)](i) but rather with a decrease in intracellular calcium pool content.
FAU - Vanoverberghe, K
AU  - Vanoverberghe K
AD  - INSERM EMI 0228, Laboratoire de Physiologie Cellulaire, Batiment SN3, Universite 
      des Sciences et Technologies de Lille, 59655 Cedex, Villeneuve d'Ascq, France.
FAU - Mariot, P
AU  - Mariot P
FAU - Vanden Abeele, F
AU  - Vanden Abeele F
FAU - Delcourt, P
AU  - Delcourt P
FAU - Parys, J B
AU  - Parys JB
FAU - Prevarskaya, N
AU  - Prevarskaya N
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Cell Calcium
JT  - Cell calcium
JID - 8006226
RN  - 0 (Calcium Channels)
RN  - 0 (ITPR1 protein, human)
RN  - 0 (Inositol 1,4,5-Trisphosphate Receptors)
RN  - 0 (Receptors, Cytoplasmic and Nuclear)
RN  - 67526-95-8 (Thapsigargin)
RN  - 8L70Q75FXE (Adenosine Triphosphate)
RN  - EC 2.7.11.13 (Protein Kinase C)
RN  - EC 3.1.4.- (Type C Phospholipases)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Adenosine Triphosphate/*metabolism/pharmacology
MH  - Calcium/*metabolism/pharmacology
MH  - Calcium Channels/drug effects/genetics/metabolism
MH  - Calcium Signaling/drug effects/*physiology
MH  - Carcinoma/*metabolism/physiopathology
MH  - Cell Division/drug effects/physiology
MH  - Cell Line, Tumor
MH  - Cytoplasm/drug effects/metabolism
MH  - Down-Regulation/drug effects/physiology
MH  - Endoplasmic Reticulum/drug effects/metabolism
MH  - Humans
MH  - Inositol 1,4,5-Trisphosphate Receptors
MH  - Intracellular Fluid/drug effects/metabolism
MH  - Male
MH  - Prostatic Neoplasms/*metabolism/physiopathology
MH  - Protein Kinase C/metabolism
MH  - Receptors, Cytoplasmic and Nuclear/genetics/metabolism
MH  - Thapsigargin/pharmacology
MH  - Type C Phospholipases/drug effects/metabolism
EDAT- 2003/05/28 05:00
MHDA- 2004/03/05 05:00
CRDT- 2003/05/28 05:00
PHST- 2003/05/28 05:00 [pubmed]
PHST- 2004/03/05 05:00 [medline]
PHST- 2003/05/28 05:00 [entrez]
AID - S0143416003000241 [pii]
AID - 10.1016/s0143-4160(03)00024-1 [doi]
PST - ppublish
SO  - Cell Calcium. 2003 Jul;34(1):75-85. doi: 10.1016/s0143-4160(03)00024-1.