Aim: We looked at the connection between autophagy and apoptosis after our prior research indicated that melatonin could cause MCF-7 and MDA-MB-231 cells in the present study.
Material and Method: In order to investigate the autophagy inhibition’s effect on the melatonin-induced BC cells’ apoptosis, melatonin and/or 3-methyladenine (3-MA, autophagy inhibitor) have been utilized. Melatonin was applied to the cells following a 5-mM 3-MA pre-cultivation. Then, apoptosis was detected by the TUNEL method. The technique for double immunofluorescence labeling was used to identify the molecular alterations in Bax/Bcl-2 expression. To evaluate the cell viability, the MTT test was used.
Results: When an autophagy inhibitor, 3-MA, and melatonin treatment were co-administered in MCF-7 cells, apoptosis was decreased, compared to melatonin treatment alone, but it was not significant. In addition, 3-MA application downregulated Bax expression compared with melatonin alone treatment. Combined therapy markedly elevated apoptosis and significantly up-regulated Bax protein in MDA-MB-231 cells.
Conclusion: Taken together, in MCF-7 cells, autophagy’s inhibition contributes to the downregulation of apoptosis, whereas increased apoptosis is seen in MDA-MB-231 cells. Inhibiting autophagy in these cells treated with melatonin could serve as a self-defense mechanism, and This might be a good strategy for breast cancer adjuvant treatment.
Health Sciences Research Support Group (SBAG) of TUBITAK
220S879
220S879
Primary Language | English |
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Subjects | Histology and Embryology |
Journal Section | Original Articles |
Authors | |
Project Number | 220S879 |
Publication Date | January 31, 2024 |
Submission Date | December 5, 2023 |
Acceptance Date | January 10, 2024 |
Published in Issue | Year 2024 Volume: 6 Issue: 1 |
Chief Editors
Assoc. Prof. Zülal Öner
Address: İzmir Bakırçay University, Department of Anatomy, İzmir, Türkiye
Assoc. Prof. Deniz Şenol
Address: Düzce University, Department of Anatomy, Düzce, Türkiye
E-mail: medrecsjournal@gmail.com
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