Endoplasmic reticulum Ca2+-homeostasis is altered in small and non-small cell lung cancer cell lines

Background: 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. 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. Methods: The intracellular
Ca2+-signaling was investigated using fluorescence microscopy and
the expression of Ca2+-regulating proteins was assessed using
Western Blot analysis. Results: In 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. Conclusion: The significant differences in
Ca2+-homeostasis between lung cancer and NHBE cells could represent
a new target for cancer treatments.