OCT4 Expression in Gliomas Is Dependent on Cell Metabolism

Author:

Volnitskiy Andrey1ORCID,Shabalin Konstantin1ORCID,Pantina Rimma1,Varfolomeeva Elena1ORCID,Kovalev Roman1,Burdakov Vladimir1,Emelianova Svetlana1,Garaeva Luiza1,Yakimov Alexander12ORCID,Sogoyan Marina3,Filatov Michael1,Konevega Andrey L.124ORCID,Shtam Tatiana145ORCID

Affiliation:

1. Petersburg Nuclear Physics Institute Named by B.P. Konstantinov of National Research Centre “Kurchatov Institute”, Orlova Roscha 1, 188300 Gatchina, Russia

2. Institute of Biomedical Systems and Biotechnologies, Peter the Great St. Petersburg Polytechnic University, Politehnicheskaya 29, 195251 St. Petersburg, Russia

3. H.Turner National Medical Research Center for Children’s Orthopedics and Trauma Surgery of the Ministry of Health of the Russian Federation, Parkovaya 64-68, Pushkin, 196603 St. Petersburg, Russia

4. National Research Center “Kurchatov Institute”, Akademika Kurchatova pl. 1, 123182 Moscow, Russia

5. Institute of Cytology, Russian Academy of Sciences, Tikhoretsky Ave. 4, 194064 St. Petersburg, Russia

Abstract

The OCT4 transcription factor is necessary to maintain cell stemness in the early stages of embryogenesis and is involved in the formation of induced pluripotent stem cells, but its role in oncogenesis is not yet entirely clear. In this work, OCT4 expression was investigated in malignant gliomas. Twenty glioma cell lines and a sample of normal adult brain tissue were used. OCT4 expression was found in all studied glioma cell lines but was not detected in normal adult brain tissue. For one of these lines, OCT4 knockdown caused tumor cell death. By varying the culture conditions of these cells, we unexpectedly found that OCT4 expression increased when cells were incubated in serum-free medium, and this effect was significantly enhanced in serum-free and L-glutamine-free medium. L-glutamine and the Krebs cycle, which is slowed down in serum-free medium according to our NMR data, are sources of α-KG. Thus, our data indicate that OCT4 expression in gliomas may be regulated by the α-KG-dependent metabolic reprogramming of cells.

Funder

Ministry of Science and Higher Education of the Russian Federation

Publisher

MDPI AG

Subject

Microbiology (medical),Molecular Biology,General Medicine,Microbiology

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