Dose-Dependent Effect of Mitochondrial Superoxide Dismutase Gene Overexpression on Radioresistance of HEK293T Cells

Marina M Tavleeva1, Elena E Rasova1, Anna V Rybak1

  • 1Institute of Biology of Komi Scientific Centre, Ural Branch of Russian Academy of Sciences, 28b Kommunisticheskaya St., Syktyvkar 167982, Russia.

Insights

Altering manganese superoxide dismutase (SOD2) expression levels impacts cell radioresistance. Moderate SOD2 overexpression enhanced viability after 2 Gy irradiation, while higher levels protected cells at 5 Gy.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Radiation Oncology

Background:

  • Gain-of-function studies on antioxidative enzymes like manganese superoxide dismutase (SOD2) yield contradictory results.
  • Gene overexpression levels significantly influence experimental outcomes in gain-of-function studies.

Purpose of the Study:

  • To investigate the effect of varying ectopic expression levels of SOD2 on the radioresistance of HEK293T cells.
  • To explore the combined effect of SOD2 and Catalase (CAT) overexpression on cellular radioresistance.

Main Methods:

  • CRISPR activation (CRISPRa) technology was employed to modulate SOD2 expression levels.
  • HEK293T cells were subjected to varying doses of irradiation (2, 3, and 5 Gy) post-transfection.
  • Cell viability and clonogenic survival assays were performed to assess radioresistance.

Main Results:

  • Moderate SOD2 overexpression increased cell viability after 2 Gy irradiation, but not at higher doses.
  • Higher SOD2 overexpression (up to 22.5-fold) enhanced cell viability specifically after 5 Gy irradiation.
  • A 15-20 fold increase in SOD2 expression improved clonogenic survival post-5 Gy irradiation.
  • Simultaneous overexpression of SOD2 and CAT provided a more effective enhancement of clonogenic survival than individual overexpression.

Conclusions:

  • The degree of SOD2 overexpression is critical for achieving a protective effect against irradiation.
  • Combined SOD2 and CAT overexpression shows potential for mitigating oxidative stress in pathological conditions.
  • The findings suggest a strategy for reducing oxidative stress via coordinated gene expression modulation.