Abstract
BackgroundKnowledge of differences in the cellular physiology of malignant and non-malignant cells is a prerequisite for the development of cancer treatments that effectively kill cancer without damaging normal cells. Calcium is a ubiquitous signal molecule that is involved in the control of proliferation and apoptosis. We aimed to investigate if the endoplasmic reticulum (ER) Ca2+-homeostasis is different in lung cancer and normal human bronchial epithelial (NHBE) cells.MethodsThe intracellular Ca2+-signaling was investigated using fluorescence microscopy and the expression of Ca2+-regulating proteins was assessed using Western Blot analysis.ResultsIn a Small Cell Lung Cancer (H1339) and an Adeno Carcinoma Lung Cancer (HCC) cell line but not in a Squamous Cell Lung Cancer (EPLC) and a Large Cell Lung Cancer (LCLC) cell line the ER Ca2+-content was reduced compared to NHBE. The reduced Ca2+-content correlated with a reduced expression of SERCA 2 pumping calcium into the ER, an increased expression of IP3R releasing calcium from the ER, and a reduced expression of calreticulin buffering calcium within the ER. Lowering the ER Ca2+-content with CPA led to increased proliferation NHBE and lung cancer cells.ConclusionThe significant differences in Ca2+-homeostasis between lung cancer and NHBE cells could represent a new target for cancer treatments.
Highlights
Knowledge of differences in the cellular physiology of malignant and non-malignant cells is a prerequisite for the development of cancer treatments that effectively kill cancer without damaging normal cells
The significant differences in Ca2+-homeostasis between lung cancer and normal human bronchial epithelial (NHBE) cells could represent a new target for cancer treatments
To investigate the role of Ca2+-influx in Ca2+-homeostasis in lung cancer cells, NHBE, H1339, HCC, EPLC 272 and Large Cell Lung Cancer (LCLC) cells were exposed to 1 mM ATP in the presence and the absence of extracellular calcium (PBS containing no calcium but 0.02% EGTA)
Summary
Knowledge of differences in the cellular physiology of malignant and non-malignant cells is a prerequisite for the development of cancer treatments that effectively kill cancer without damaging normal cells. One of the main reasons for the failure of therapeutic regimens is the fact that cancer cells originate from normal cells and possess similar characteristics. This means that anti-cancer therapies inevitably affect the normal cell population and these side effects often hinder more effective treatments. Calcium is a ubiquitous signal molecule that is involved in almost all cellular pathways [2,3].
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