Fig. 6: SIRT1 inactivation increases apoptosis and therapeutic efficacy in KRASMut cells.
From: Oncogenic KRAS mutation confers chemoresistance by upregulating SIRT1 in non-small cell lung cancer
A, B and D, E H358 cells were transfected with siCon or siSIRT1 (80 nM) and then seeded into 96-well plates for a growth assay A, D and into 12-well plates on agarose gel for a colony formation assay B, E. A, B without erlotinib; D, E dose-dependent treatment with erlotinib. Student’s t test, mean ± SD; n = 6; *p < 0.05. C H358, A427, and H727 cells were transfected with siCon or siSIRT1 (80 nM) and then immunoblotted with anti-SIRT1, anti-pMEK, anti-MEK, anti-pERK, anti-ERK, anti-pAkt, anti-Akt, anti-pEGFR, anti-EGFR, anti-pSTAT3, anti-STAT3, and anti β-actin antibodies. F–H H358 cells were transfected with siCon or siSIRT1 (80 nM) and treated with erlotinib (10 μM). F Cell lysates were immunoblotted with anti-PARP and anti-caspase-3 antibodies. G Cells treated with the drugs were subjected to immunofluorescence staining and H analysis of DNA damage using the APO-BrdU TUNEL assay.
