Fig. 3

The endoplasmic reticulum stress might be responsible for the apoptosis and stemness reduction mediated by MCL-1 in MSLC. a MCL-1 silencing upregulated the expression of ER stress-associated genes in MSLC but not in non-MSLC. At 24 h after transfection of MCL-1-siRNA in MSLC and non-MSLC, quantitative real-time PCR was used to evaluate the expression levels of ER stress-associated genes (**p < 0.01). The MCL-1-siRNA-scrambled was used as a control (control miRNA). b–d MSLC was treated with ER stress agonist tunicamycin (3 μg/mL) for 24 h followed by evaluating the cell viability and apoptosis using MTS assay, annexin V assay, and caspase 3/7 activity detection, respectively. e Influence of tunicamycin on CSC-associated gene in MSLC. Cells were treated with 3 μg/mL of tunicamycin for 24 h, and then the CSC-associated genes in MSLC were assessed. f MCL-1 was induced by tunicamycin in MSLC but not in non-MSLC. The cells were subjected to tunicamycin (3 μg/mL) treatment for 24 h followed by detecting the MCL-1 mRNA content