AI Article Synopsis
- Cells derived from PC3 exhibit varying levels of resistance to the Ca(2+)-ATPase inhibitor thapsigargin (TG), with some showing a resistance increase up to 1350-fold.
- Overexpression of SERCA2 is present in all resistant PC3/TG cells, contributing to TG resistance, but other mechanisms are also at play, particularly in the most resistant cells.
- In contrast, DU145/TG cells do not overexpress SERCA and maintain TG resistance, suggesting distinct resistance mechanisms that do not involve other transport or anti-apoptotic proteins.
Article Abstract
Cells with increasing resistance to the sarcoplasmic/endoplasmic reticulum Ca(2+)-ATPase (SERCA) inhibitor thapsigargin (TG), ranging from 60-fold (PC3/TG(10) cells) to 1350-fold (PC3/TG(2000) cells), were derived from PC3 cells. SERCA2 is overexpressed in all PC3/TG cells but retains sensitivity to TG. siRNA-mediated downregulation of SERCA completely or partially reverses TG resistance in PC3/TG(10) or PC3/TG(2000) cells, respectively; thus SERCA overexpression mediates resistance in PC3/TG(10) cells but is not the only resistance mechanism in PC3/TG(2000) cells. By contrast, SERCA is not overexpressed in TG-resistant DU145/TG cells derived from DU145 cells. DU145/TG cells retain resistance while in PC3/TG cells resistance decreases upon removal of TG selection. The transport proteins PGP/BCRP/MRP1 and anti-apoptotic proteins Bcl2/Bcl(XL) are not involved in mediating resistance in either cell line. PARP and caspase 3 cleavage in response to other drugs demonstrate that the apoptotic pathways tested remain intact in these cells. Further, no cross-resistance occurs to other drugs. Thus, novel TG-specific resistance mechanisms are recruited by these cancer cells.
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| http://dx.doi.org/10.1016/j.abb.2007.03.040 | DOI Listing |
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