Fig. 5: YME1L silencing impairs mitochondrial functions in OS cells.
From: Targeting the mitochondrial protein YME1L to inhibit osteosarcoma cell growth in vitro and in vivo
The patient-derived primary OS cells (pOS-1), with the lentiviral YME1L shRNA (“shYME1L-seq1/shYME1L-seq2”, representing two different shRNAs) or scramble control shRNA (“shC”), were established and cultivated for 48 h, mitochondrial depolarization (by testing JC-1 green monomers intensity, A), ROS production (by measuring CellROX/DCF-DA intensity, B and C), ssDNA contents (D) and lipid peroxidation (by measuring TBAR activity, E), as well as the mitochondrial respiratory chain complex I (mito-complex I) activity (F) and ATP contents (G) were measured. The primary OS cells that were derived two other patients, pOS-2 and pOS-3 or the immortalized U2OS cells, with lentiviral shYME1L-seq2 or shC, were cultivated for 48 h, ROS production (CellROX intensity, H) or ATP contents (I) were measured. Data were presented as mean ± standard deviation (SD, n = 5). *P < 0.001 versus “shC” group. Each single experiment was repeated for five times. Scale bar = 100 μm.
