Pseurotin D Induces Apoptosis through Targeting Redox Sensitive Pathways in Human Lymphoid Leukemia Cells

Investor logo

Warning

This publication doesn't include Faculty of Sports Studies. It includes Faculty of Science. Official publication website can be found on muni.cz.
Authors

MOSEJOVÁ Eva BOSNJAKOVIC Rebeka KUBALA Lukáš VAŠÍČEK Ondřej

Year of publication 2021
Type Article in Periodical
Magazine / Source Antioxidants
MU Faculty or unit

Faculty of Science

Citation
Web https://www.mdpi.com/2076-3921/10/10/1576
Doi http://dx.doi.org/10.3390/antiox10101576
Keywords pseurotin D; proliferation; apoptosis; mitochondrial activity; reactive oxygen species; lymphoma
Description Chronic lymphocytic leukemia (CLL) is the most prevalent lymphoid malignancy in many geographical regions of the world. Pseurotin D, a secondary metabolite of fungi, represents a group of bioactive natural products with a newly ascribed range of interesting biological activities. The purpose of this study was to bring new insights into the mechanism behind the effects of pseurotin D on MEC-1 cells as a representative CLL cell line, with a particular focus on selected signaling pathways important in the proliferation of cells and targeting mitochondrial metabolism. Our results showed that pseurotin D was able to significantly inhibit the proliferation of MEC-1 cells and arrested them in the G2/M cell cycle phase. In addition, pseurotin D was able to induce apoptosis. We found that all of these effects were associated with a change in mitochondrial membrane potential and the production of mitochondrial reactive oxygen species (ROS). We showed for the first time that pseurotin D suppresses MEC-1 cell proliferation and induces apoptotic cell death via induction of the collapse of the mitochondria respiratory chain and the ROS-related caspase pathway. Our results show the pseurotins family as promising compounds which could serve as a basis for the development of new compounds in the treatment of lymphoma.
Related projects:

You are running an old browser version. We recommend updating your browser to its latest version.

More info