Cross-talk between NFκB and PI3-kinase/AKT pathway in PEL cell lines.

<p>(<b>A</b>) <b>Bay11-7085 treatment inactivates AKT and its down-stream targets in PEL cells.</b> BC1 and BC3 cells were treated with 5 and 10 µM Bay11-7085 for 24 hours. Cells were lysed and equal amounts of proteins were separated by SDS-PAGE, transferred to PVDF membrane, and immunoblotted with antibodies against p-AKT, p-FOXO1, p-GSK3, p-Bad and Beta-actin. (<b>B</b>) <b>Transcriptional knock down of p65 causes in-activation of AKT and its down-stream targets in PEL cells.</b> BC1 and BC3 cells were transfected with siRNA against p65 for 48 hours. Following transfection, cells were lysed and equal amounts of proteins were separated by SDS-PAGE, transferred to PVDF membrane, and immunoblotted with antibodies against p-AKT, p-FOXO1, p-GSK3, p-Bad and Beta-actin. (<b>C</b>) <b>Transcriptional targeting of AKT causes in-activation of NFκB pathway.</b> BC1 cells were transfected with siRNA against AKT for 48 hours. Following transfection, cells were lysed and equal amounts of proteins were separated by SDS-PAGE, transferred to PVDF membrane, and immunoblotted with antibodies against p-AKT, p-IκBα and Beta-actin.