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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
1

Effect of the m-3M3FBS on Ca2+ movement in human SCM1 gastric cancer cells

Lee, Hsiao-ying 28 March 2011 (has links)
m-3M3FBS is a new compound that has been used as a phospholipase C (PLC) activator. The effect of m-3M3FBS on cytosolic free Ca2+ concentrations in human gastric cancer cells (SCM1) is unclear. This study explored whether m-3M3FBS changed basal [Ca2+]i levels in suspended SCM1 cells by using fura-2 as a Ca2+-sensitive fluorescent dye. m-3M3FBS at concentrations between 1-50 £gM increased [Ca2+]i in a concentration-dependent manner. The Ca2+ signal was reduced partly by removing extracellular Ca2+. This Ca2+ influx was inhibited by phospholiapase A2 inhibitor aristolochic acid , store-operated Ca2+ channel blockers nifedipine ¡B econazole and SK&F96365; and protein kinase C inhibitor GF109203X. Phorbol 12-myristate 13-acetate ([PMA] a protein kinase C activator) had no effect on m-3M3FBS-induced [Ca2+]i rise. In Ca2+-free medium , pretreatment with m-3M3FBS abolished thapsigargin (TG) or 2,5-di-tert-butylhydroquinone (BHQ) - induced [Ca2+]i rise. Conversely, pretreatment with the endoplasmic reticulum Ca2+ pump inhibitors TG or BHQ partly inhibited m-3M3FBS -induced Ca2+ release. The inhibition of PLC with U73122 did not alter mMIRC. Collectively, in SCM1 cells, mMIRC by causing PLCindependent Ca2+ release from the endoplasmic reticulum and Ca2+ influx via phospholipase A2-protein kinase C-sensitive store-operated Ca2+ channels.

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