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@article{1397077,
author = {Chovancova, Barbora and Hudecova, Sona and Lencesova, Lubomira and Babula, Petr and Rezuchova, Ingeborg and Penesova, Adela and Grman, Marian and Moravcik, Roman and Zeman, Michal and Krozanova, Olga},
article_location = {Basel},
article_number = {2},
doi = {http://dx.doi.org/10.1159/000485290},
keywords = {Melatonin; Apoptosis; ER-stress; Cancer; Calcium; Reactive oxygen species},
language = {eng},
issn = {1015-8987},
journal = {Cellular Physiology and Biochemistry},
title = {Melatonin-Induced Changes in Cytosolic Calcium Might be Responsible for Apoptosis Induction in Tumour Cells},
volume = {44},
year = {2017}
}
TY - JOUR
ID - 1397077
AU - Chovancova, Barbora - Hudecova, Sona - Lencesova, Lubomira - Babula, Petr - Rezuchova, Ingeborg - Penesova, Adela - Grman, Marian - Moravcik, Roman - Zeman, Michal - Krozanova, Olga
PY - 2017
TI - Melatonin-Induced Changes in Cytosolic Calcium Might be Responsible for Apoptosis Induction in Tumour Cells
JF - Cellular Physiology and Biochemistry
VL - 44
IS - 2
SP - 763-777
EP - 763-777
PB - Karger
SN - 10158987
KW - Melatonin
KW - Apoptosis
KW - ER-stress
KW - Cancer
KW - Calcium
KW - Reactive oxygen species
N2 - Melatonin is a hormone transferring information about duration of darkness to the organism and is known to modulate several signaling pathways in the cells, e.g. generation of endoplasmic reticulum stress, oxidative status of the cells, etc. Melatonin has been shown to exert antiproliferative and cytotoxic effects on various human cancers. We proposed that this hormone can differently affect tumour cells and healthy cells. Methods: We compared the effect of 24 h melatonin treatment on calcium transport (by fluorescent probes FLUO-3AM and Rhod-5N), ER stress (determined as changes in the expression of CHOP, XBP1 and fluorescently, using Thioflavin T), ROS formation (by CellROX® Green/Orange Reagent) and apoptosis induction (by Annexin-V-FLUOS/propidiumiodide) in two tumour cell lines – ovarian cancer cell line A2780 and stable cell line DLD1 derived from colorectal carcinoma, with non-tumour endothelial cell line EA.hy926. Results: Melatonin increased apoptosis in both tumour cell lines more than twice, while in EA.hy926 cells the apoptosis was increased only by 30%. As determined by silencing with appropriate siRNAs, both, type 1 sodium/calcium exchanger and type 1 IP3 receptor are involved in the apoptosis induction. Antioxidant properties of melatonin were significantly increased in EA.hy926 cells, while in tumour cell lines this effect was much weaker. Conclusion: Taken together, melatonin has different antioxidative effects on tumour cells compared to non-tumour ones; it also differs in the ability to induce apoptosis through the type 1 sodium/calcium exchanger, and type 1 IP3 receptor. Different targeting of calcium transport systems in tumour and normal, non-tumour cells is suggested as a key mechanism how melatonin can exert its anticancer effects. Therefore, it might have a potential as a novel therapeutic implication in cancer treatment.
ER -
CHOVANCOVA, Barbora, Sona HUDECOVA, Lubomira LENCESOVA, Petr BABULA, Ingeborg REZUCHOVA, Adela PENESOVA, Marian GRMAN, Roman MORAVCIK, Michal ZEMAN and Olga KROZANOVA. Melatonin-Induced Changes in Cytosolic Calcium Might be Responsible for Apoptosis Induction in Tumour Cells. \textit{Cellular Physiology and Biochemistry}. Basel: Karger, 2017, vol.~44, No~2, p.~763-777. ISSN~1015-8987. Available from: https://dx.doi.org/10.1159/000485290.
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