Fig. 3

Atrovastatin sensitizes chemotherapy through modulating NF-κB a CMap approach to identify chemosensitizer drugs using two different signatures: i) down-regulated genes by ITGB3 depletion, and ii) the intersection of i) and NF-κB pathway genes b the candidate drug list predicted by the two signatures. Atorvastatin was commonly predicted by both signatures. c and d Immunoblotting analysis for cleaved caspase 3 or (C.Caspase3 or C.Caspase9) at indicative dose c of atorvastatin (ATV) or Days (d, with 0.1 μM of ATV) with doxorubicin (Doxo). α-tubulin or β-actin for equal loading control e Light microscopic images of TD cells with or without atorvastatin (ATV, 1 μM) after doxorubicin treatment (Doxo) (top), Graphical presentation of cell viability (bottom) f Flow cytometry for Annexin V staining at 24 h after indicative dose of Doxorubicin (Doxo) with 0.1 μM of ATV pretreatment (top), Graphical presentation of apoptotic cells (bottom) g Luciferase reporter activity for NF-κB activity in TD after indicative dose of atorvastatin (ATV) h Immunoblotting analysis for ITGB3, BCL-xL and IκB after indicative dose of atorvastatin (ATV) treatment in TD cells, β-actin for equal loading control