Paclitaxel induces apoptosis in breast cancer cells through different calcium - regulating mechanisms depending on external calcium condition

Zhi Pan, Andrew Avila, Lauren Gollahon

Research output: Contribution to journalArticlepeer-review

Abstract

Previously, we reported that endoplasmic reticulum calcium stores were a direct target for paclitaxel initiation of apoptosis. Furthermore, the actions of paclitaxel attenuated Bcl-2 resistance to apoptosis through endoplasmic reticulum-mediated calcium release. To better understand the calcium-regulated mechanisms of paclitaxel-induced apoptosis in breast cancer cells, we investigated the role of extracellular calcium, specifically; whether influx of extracellular calcium contributed to and/or was necessary for paclitaxel-induced apoptosis. Our results demonstrated that paclitaxel induced extracellular calcium influx. This mobilization of extracellular calcium contributed to subsequent cytosolic calcium elevation differently, depending on dosage. Under normal extracellular calcium conditions, high dose paclitaxel induced apoptosis-promoting calcium influx, which did not occur in calcium-free conditions. In the absence of extracellular calcium an “Enhanced Calcium Efflux” mechanism in
Original languageEnglish
Pages (from-to)2672-2694
JournalInternational Journal of Molecular Science
StatePublished - Feb 17 2014

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