Tamoxifen-induced [Ca2+]i rises and Ca2+-independent cell death in human oral cancer cells

Sau Tung Chu, Chorng Chih Huang, Chun Jen Huang, Jin Shiung Cheng, Kuo Liang Chai, He Hsiung Cheng, Yi Chien Fang, Chao Chuan Chi, Hsing Hao Su, Chiang Ting Chou, Chung Ren Jan*

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

13 Scopus citations


The purpose of this study was to explore the effect of tamoxifen on cytosolic free Ca2+ concentrations ([Ca2+]i) and cell viability in OC2 human oral cancer cells. [Ca2+]i and cell viability were measured by using the fluorescent dyes fura-2 and WST-1, respectively. Tamoxifen at concentrations above 2 μM increased [Ca2+]i in a concentration-dependent manner. The Ca2+ signal was reduced partly by removing extracellular Ca2+. The tamoxifen-induced Ca2+ influx was sensitive to blockade of L-type Ca2+ channel blockers but insensitive to the estrogen receptor antagonist ICI 182,780 and protein kinase C modulators. In Ca2+-free medium, after pretreatment with 1 μM thapsigargin (an endoplasmic reticulum Ca2+ pump inhibitor), tamoxifen-induced [Ca2+]i rises were substantially inhibited; and conversely, tamoxifen pretreatment inhibited a part of thapsigargin-induced [Ca2+]i rises. Inhibition of phospholipase C with 2 μM U73122 did not change tamoxifen-induced [Ca2+]i rises. At concentrations between 10 and 50 μM tamoxifen killed cells in a concentration-dependent manner. The cytotoxic effect of 23 μM tamoxifen was not reversed by prechelating cytosolic Ca2+ with BAPTA. Collectively, in OC2 cells, tamoxifen induced [Ca2+]i rises, in a nongenomic manner, by causing Ca2+ release from the endoplasmic reticulum, and Ca2+ influx from L-type Ca2+ channels. Furthermore, tamoxifen-caused cytotoxicity was not via a preceding [Ca2+]i rise.

Original languageEnglish
Pages (from-to)353-367
Number of pages15
JournalJournal of Receptors and Signal Transduction
Issue number5-6
StatePublished - 09 2007
Externally publishedYes


  • Ca
  • Fura-2
  • Oral cancer cells
  • Tamoxifen
  • Thapsigargin


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