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. 2021 Jul 22;22(3):680. doi: 10.3892/ol.2021.12941

Figure 4.

Figure 4.

Necrostatin-1 and NAC suppress cytotoxicity enhanced by BTZ plus RCS in CAL27 and Detroit562 cells. (A) CAL27 and Detroit562 cells were untreated or treated with BTZ (5 nM for CAL27 cells, 10 nM for Detroit562 cells) and/or RCS (5 µM for CAL27 cells, 10 µM for Detroit562 cells) in the presence or absence of necrostatin-1 (25 and 50 µM) for 24 and 48 h. Viable cell number was determined by the CellTiter Blue assay. *P<0.05 and **P<0.01 vs. cells not treated with necrostatin-1. (B) CAL27 and Detroit562 cells were untreated or treated with BTZ in the presence or absence of RCS for 24 and 48 h followed by immunoblotting. HT-29 cells treated with Z-VAD-fmk, cycloheximide and TNF-α were a positive control for induction of necroptosis. Immunoblotting with anti-β-actin mAb was performed as a loading control. NAC, N-acetyl-L-cysteine; RCS, ricolinostat; BTZ, bortezomib; RIPK1, serine/threonine-protein kinase 1; MLKL, mixed lineage kinase domain-like protein.