Research Paper Volume 13, Issue 12 pp 15833—15874

The lack of functional DNMT2/TRDMT1 gene modulates cancer cell responses during drug-induced senescence

DNMT2/TRDMT1 gene knockout modulated DOX- and ETOPO-induced senescence program in glioblastoma cells as judged by affected SIPS response (lowered number of SA-beta-gal-positive cells and diminished levels of nuclear p21), apoptosis resistance, increased ROS production, increased DSBs, impaired RNA-mediated DDR and autophagic response, modulated SASP and the levels of NSUN proteins. Thus, DNMT2/TRDMT1 gene knockout may result in the promotion of some selected adverse side effects mediated by drug-stimulated senescence.

Figure 9. DNMT2/TRDMT1 gene knockout modulated DOX- and ETOPO-induced senescence program in glioblastoma cells as judged by affected SIPS response (lowered number of SA-beta-gal-positive cells and diminished levels of nuclear p21), apoptosis resistance, increased ROS production, increased DSBs, impaired RNA-mediated DDR and autophagic response, modulated SASP and the levels of NSUN proteins. Thus, DNMT2/TRDMT1 gene knockout may result in the promotion of some selected adverse side effects mediated by drug-stimulated senescence.