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.

Základní údaje

Originální název

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

Autoři

CHOVANCOVA, Barbora (703 Slovensko), Sona HUDECOVA (703 Slovensko), Lubomira LENCESOVA (703 Slovensko), Petr BABULA (203 Česká republika, garant, domácí), Ingeborg REZUCHOVA (703 Slovensko), Adela PENESOVA (703 Slovensko), Marian GRMAN (703 Slovensko), Roman MORAVCIK (703 Slovensko), Michal ZEMAN (703 Slovensko) a Olga KROZANOVA (703 Slovensko)

Vydání

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

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

30105 Physiology

Stát vydavatele

Švýcarsko

Utajení

není předmětem státního či obchodního tajemství

Impakt faktor

Impact factor: 5.500

Kód RIV

RIV/00216224:14110/17:00098524

Organizační jednotka

Lékařská fakulta

UT WoS

000418611700026

Klíčová slova anglicky

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

Štítky

Příznaky

Mezinárodní význam, Recenzováno
Změněno: 17. 5. 2018 17:18, Soňa Böhmová

Anotace

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.