J 2017

Melatonin-Induced Changes in Cytosolic Calcium Might be Responsible for Apoptosis Induction in Tumour Cells

CHOVANCOVA, Barbora, Sona HUDECOVA, Lubomira LENCESOVA, Petr BABULA, Ingeborg REZUCHOVA et. al.

Basic information

Original name

Melatonin-Induced Changes in Cytosolic Calcium Might be Responsible for Apoptosis Induction in Tumour Cells

Authors

CHOVANCOVA, Barbora (703 Slovakia), Sona HUDECOVA (703 Slovakia), Lubomira LENCESOVA (703 Slovakia), Petr BABULA (203 Czech Republic, guarantor, belonging to the institution), Ingeborg REZUCHOVA (703 Slovakia), Adela PENESOVA (703 Slovakia), Marian GRMAN (703 Slovakia), Roman MORAVCIK (703 Slovakia), Michal ZEMAN (703 Slovakia) and Olga KROZANOVA (703 Slovakia)

Edition

Cellular Physiology and Biochemistry, Basel, Karger, 2017, 1015-8987

Other information

Language

English

Type of outcome

Článek v odborném periodiku

Field of Study

30105 Physiology

Country of publisher

Switzerland

Confidentiality degree

není předmětem státního či obchodního tajemství

Impact factor

Impact factor: 5.500

RIV identification code

RIV/00216224:14110/17:00098524

Organization unit

Faculty of Medicine

UT WoS

000418611700026

Keywords in English

Melatonin; Apoptosis; ER-stress; Cancer; Calcium; Reactive oxygen species

Tags

Tags

International impact, Reviewed
Změněno: 17/5/2018 17:18, Soňa Böhmová

Abstract

V originále

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.