Effect of NPC15199 on [Ca²⁺]i and viability in SCM1 human gastric cancer cells.

  title={Effect of NPC15199 on [Ca²⁺]i and viability in SCM1 human gastric cancer cells.},
  author={He-Hsiung Cheng and C T Chou and Wei-Zhe Liang and Jin‐shiung Cheng and Hong‐Tai Chang and Chun‐Chi Kuo and I-shu Chen and Ti Lu and C.-C. Yu and Fu-An Chen and Daih Huang Kuo and Pochuen Shieh and C-R Jan},
  journal={The Chinese journal of physiology},
  volume={59 5},
NPC15199 is a synthesized compound that inhibits inflammation in some models. However, whether NPC15199 affects Ca²⁺ homeostasis in human gastric cancer is unclear. This study examined the effect of NPC15199 on cytosolic free Ca²⁺ concentrations ([Ca²⁺]i) and viability in SCM1 human gastric cancer cells. The Ca²⁺-sensitive fluorescent dye fura-2 was used to measure [Ca²⁺]i. NPC15199 evoked [Ca²⁺]i rises concentration-dependently. The response was reduced by removing extracellular Ca²⁺. NPC15199… 

Figures from this paper



Thimerosal-induced apoptosis in human SCM1 gastric cancer cells: activation of p38 MAP kinase and caspase-3 pathways without involvement of [Ca2+]i elevation.

The results suggest that in SCM1 cells, thimerosal caused Ca2+-independent apoptosis via phosphorylating p38 MAPK resulting in caspase-3 activation.

NPC-15199, a novel anti-inflammatory agent, mobilizes intracellular Ca2+ in bladder female transitional carcinoma (BFTC) cells.

The findings suggest that in BFTC bladder cancer cells, NPC-15199 induced Ca2- release from the endoplasmic reticulum and activating Ca2+ entry.

Effect of NPC-15199 on Ca2+ levels in renal tubular cells.

The results suggest that NPC-15199 rapidly increases [Ca2+]i by stimulating both extracellular Ca 2+ influx and intracellular Ca2+ release via as yet unidentified mechanism(s).

Effect of caffeic acid on Ca2+ homeostasis and apoptosis in SCM1 human gastric cancer cells

Collectively, in SCM1 cells, caffeic acid-induced [Ca2+]i rises by evoking phospholipase C-dependent Ca2+ release from the endoplasmic reticulum and Ca2- entry via store-operated Ca2+.

Inhibition of calcium-independent phospholipase A2 suppresses proliferation and tumorigenicity of ovarian carcinoma cells.

An essential role is shown for iPLA2 in cell cycle progression and tumorigenesis of ovarian carcinoma cells through G2/M-phase arrest.

Suppression of Tumor Formation by a Cyclooxygenase-2 Inhibitor and a Peroxisome Proliferator-Activated Receptor γ Agonist in an In vivo Mouse Model of Spontaneous Breast Cancer

The findings suggest that a combination of a COX-2 inhibitor and PPARγ agonist can delay breast cancer in a mouse model and suggest that these agents should be studied in the context of human populations with high breast cancer risk.

Inhibition of Rat Mammary Gland Carcinogenesis by Simultaneous Targeting of Cyclooxygenase-2 and Peroxisome Proliferator-activated Receptor γ

Combining both agents exerted higher cancer inhibition than separate treatments and simultaneous targeting of COX-2 and PPARγ may inhibit mammary cancer development more effectively than targeting each molecule alone.

Thapsigargin, a tumor promoter, discharges intracellular Ca2+ stores by specific inhibition of the endoplasmic reticulum Ca2(+)-ATPase.

The results suggest that thapsigargin increases the concentration of cytosolic free Ca2+ in sensitive cells by an acute and highly specific arrest of the endoplasmic reticulum Ca 2+ pump, followed by a rapid Ca2+.

Purinergic signalling and cancer

The evidence presented in this review, most of which is based on in vitro studies, although with a limited amount from in vivo experiments and human studies, warrants further efforts to explore the therapeutic potential of purinoceptor targeting in cancer.