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See Latest ArticlesAltered Ca2+-homeostasis of cisplatin-treated and low level resistant non-small-cell and small-cell lung cancer cells
Cellular Oncology, 07/29/09
Schrödl K et al. – Study concludes that cisplatin therapy leads to a decreased Ca2+-content of the endoplasmic reticulum (ER) thereby inducing low level resistance. This is caused by upregulation of the inositol-1,4,5-trisphosphate receptor (IP3R) in squamous cell lung carcinoma cell line EPLC and decreased expression of sarco/endoplasmic reticulum Ca2+-ATPases (SERCA) in small cell lung cancer cell line H1339.
Methods- Study aims to investigate if:
- Treatment with cisplatin alters the intracellular Ca2+-homeostasis of lung cancer cells, and
- How this may be related to cisplatin resistance
- EPLC M1 and H1339 cells were exposed to cisplatin analogue to the in vivo pharmacokinetics
- Changes in the cytoplasmic Ca2+-concn were recorded using fluorescence microscopy
- Protein expression was quantified using IFC and Western Blot analysis
- Changes in gene expression were accomplished by siRNA techniques
- Four “cycles” of cisplatin led to low level resistance in EPLC and H1339 cells
- In the low level resistant cell clones, the Ca2+-content of ER was decreased
- In low level resistant EPLC cells, this was correlated with an increased expression of the IP3R
- This could be reversed by inhibiting the increased expression of IP3R by siRNA
- In low level resistant H1339 cells, the decreased Ca2+-content of the ER was correlated with a decreased expression of SERCA
- Decreasing the expression of SERCA in naïve H1339 cells resulted in low level cisplatin resistance
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