Conclusions
The results indicated that TSR2-induced apoptosis was mediated by inhibiting the NF-κB signaling pathway, which may provide an effective target in gene therapy for LSCC. Level of evidence: NA. Laryngoscope, 128:E130-E134, 2018.
Methods
We investigated the expression level of TSR2 in LSCC tissues and cells by performing quantitative real-time polymerase chain reaction (qRT-PCR). The pcDNA3.1-TSR2 was constructed to explore the effect of overexpressing TSR2 in Hep-2 cells and AMC-HN-8 cells. We further investigated the effect of overexpressing TSR2 on cell apoptosis-related protein and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) p65 nuclear translocation through Western blot and terminal dUTP nick end-labeling assays.
Results
We found that TSR2 was downregulated in LSSC tissues and cells compared with the controls, and the overexpression of TSR2 in Hep-2 and AMC-HN-8 cells could promote cell apoptosis and related apoptosis proteins. The Western blot/qRT-PCR data further indicated that overexpression of TSR2 in Hep-2 and AMC-HN-8 cells could lead to a block of NF-κB signaling pathway via decreasing nuclear NF-κB p65 and increasing cytoplasm NF-κB p65. Moreover, overexpression of TSR2 significantly inhibited the phosphorylation of IκBα and IKKα/β. Conclusions: The results indicated that TSR2-induced apoptosis was mediated by inhibiting the NF-κB signaling pathway, which may provide an effective target in gene therapy for LSCC. Level of evidence: NA. Laryngoscope, 128:E130-E134, 2018.