Molecular mechanisms of different sensitivity of tumor cells to dexamethasone

Bulletin of Experimental Biology and Medicine
A S DukhaninE A Dukhanina

Abstract

The response of two cell lines, CSML-0 (does not express metastasin) and CSML-100 (high expression of metastasin) to cytolytic action of glucocorticoid was studied. Dexamethasone (1 microM) induced apoptosis of CSML-0 cells, while CSLM-100 cells were resistant to its cytolytic action. Apoptotic death of CSLM-100 cells was induced by incubation with dexamethasone in the presence of Ca-ATPase inhibitors, vanadate or thapsigargin. Metastasin, a proteins of the S-100 family, activated Ca-ATPase and ATP-dependent Ca2+ transport in plasmolemmal fraction of CSML-100 cells. Experiments showed that metastasin-induced activation of Ca-ATPase is a possible mechanisms of CSML-100 cell resistance to cytolytic dexamethasone action.

Citations

Nov 26, 2008·Bulletin of Experimental Biology and Medicine·E A DukhaninaL P Sashchenko
May 4, 2017·Oncotarget·Tao ChengDongming Zhou
Nov 26, 2008·Bulletin of Experimental Biology and Medicine·E A DukhaninaL P Sashchenko

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis