Fig. 2: ΔNp63α knockdown causes HNSCC more sensitive to bortezomib and vice versa for ΔNp63α overexpression.
From: ΔNp63α promotes Bortezomib resistance via the CYGB–ROS axis in head and neck squamous cell carcinoma
A. After three interfering sequence lentiviruses were transfected into HN31 cells, ΔNp63α mRNA levels of these three cell strains were detected by qPCR, indicating that the knockdown efficiency of sequence 2 was the most obvious. And the results were verified by western blot. **P < 0.01. B. UMSCC-17B cell was transfected with lentivirus and overexpressed ΔNp63α, and it was verified by qPCR and Western blot that the stably transfected strain had an obvious overexpression effect. C. HN31-shΔNp63α and 17B-LvΔNp63α were observed for ΔNp63α by immunostaining with antibody (red). Nuclei are counterstained with DAPI (blue). Scale bar: 20 μm. D. HN31-shΔNp63α, HN31-shNon, 17B-LvΔNp63α, and 17B-LvNon cells were treated with increasing concentrations of bortezomib (0.01–10000 nM) for 24 h, and IC50 was calculated using CCK-8 assay. E. 17B-R (17B-R-10nM) cells were also transfected with shRNA to knockdown ΔNp63α and the result was verified by western blot. F IC50 of 17B-R- shΔNp63α and 17B-R-shNon was calculated using the CCK-8 assay.
