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Death Mechanism of Breast Adenocarcinoma Cells, Caused by BRET-Induced Cytotoxicity of miniSOG, Depends on Intracellular Localization of Hybrid Protein NanoLuc-miniSOG
 
PIIS086956520002961-0-1
DOI10.31857/S086956520002961-0
Publication type Article
Status Published
Authors
Elena Shramova 
Affiliation: Shemyakin & Ovchinnikov Institute of Bioorganic Chemistry, RAS
Address: Russian Federation, Moscow
Galina Proshkina
Affiliation: Shemyakin & Ovchinnikov Institute of Bioorganic Chemistry, RAS
Address: Russian Federation, Moscow
S. Deyev
Affiliation:
Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, RAS
Lobachevsky State University of Nizhni Novgorod
Address: Russian Federation, Moscow
R. Petrov
Affiliation: Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, RAS
Address: Russian Federation, Moscow
Journal nameDoklady Akademii nauk
EditionVolume 482 Issue 6
Pages732-735
Abstract

Photodynamic therapy (PDT) is widely used in clinical practice to influence neoplasms in the presence of a photosensitizer, oxygen and light source. The main problem of PDT of deep tumors is the problem of delivering excitation light (without lost of its intensity) inside the body. An alternative to external light sources can be "internal" light sources based on bioluminescent systems of luciferase-substrate. In our work, as an internal light source, we used the NanoLuc-furimazine system. This system can be successfully used to excite the protein photosensitizer miniSOG and to induce the photo toxicity of this flavoprotein in cancer cells during bioluminescent resonance energy transfer (BRET). It was shown that the mechanism of cell death caused by BRET-induced phototoxicity of mimiSOG in the presence of furimazine depends on the intracellular localization of the NanoLuc-miniSOG fusion protein: BRET-mediated activation of miniSOG in mitochondrial localization causes apoptosis, while membrane localization of PS causes necrosis of cancer cells.

Keywords
Received07.12.2018
Publication date13.12.2018
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