Figure 6.
CES2 induces oxidative stress, mitochondrial dysfunction and apoptosis in OSCC. (A–B) The mitochondrial morphology was affected by CES2 as shown via TEM (A) and by stained with MitoTracker Red, as visualized via a laser confocal microscopy (B). (C) The mtDNA contents in CAL33 and UM1 cells with empty vector or CES2 overexpression were examined by qPCR. (D–F) The mitochondrial membrane potential (D), ROS levels (E) and number of apoptotic CAL33 and UM1 cells with empty vector or CES2 overexpression (F) were determined by flow cytometry. (G–J) The oxygen consumption rate (OCR) in basal and maximal-uncoupled states and mitochondrial ATP production in CAL33 and UM1 cells with CES2 or empty vector overexpression were determined with a Seahorse XF analyzer. (K–M) The mtDNA contents (K), mitochondrial membrane potential (L) and number of apoptotic cells (M) HSC3 and CAL27 cells with NC or CES2 silencing (si-1 and si-2). The mean ± s.d.; ∗, P < 0.05; Student’s t tests.