Another technique will be to target the EGFR with other agents that may reduce the oncogenic function, independent of the kind of mutation. An illustration is cetuximab. Recently, the addition of ATP-competitive HSP90 inhibitor cetuximab to afatinib has produced remarkable results in treating EGFR reversible TKI resistant lung cancer as a result of T790M mutation. EGFR specific siRNAs might be good candidates for cancer treatment because of their uniqueness, performance, and strength in gene specific silencing and ability to suppress EGFR expression independent of the mutation position of the gene. Currently, there are only a few reports on the effects of EGFR siRNAs on lung cancer cells. used a commercial EGFR wild-type siRNA pool that effectively caused the molecule caspase 3 at 96 h post transfection. The siRNA therapy also suppressed viability in H1975 cells expressing a T790M mutant EGFR and H1650 cells harboring a downstream carcinoid syndrome PTEN mutation, although not in H358 cells which can be wild-type for EGFR. In the present study, we have shown an EGFR specific siRNA is very effective at controlling the expression of EGFR in every cell lines tested, independent of the EGFR mutation status. We’ve also found that all cell lines were variably inhibited in their development from the siRNA and that the siRNA induced apoptosis in a doseand time dependent fashion, upon transfection with siRNAs targeting wild type EGFR. Our answers are partly in discordance with the information of Sordella et al. who, although using unique siRNA sequences and finding assays, discovered no biological effects in wild-type cells. These differences may possibly reside in the focus of the siRNAs used and the capability of the siRNAs to reduce gene expression that has been large and uniform across cell lines in our experiments. Our results are in line with the report of Rothenberg et al., which confirmed that lentivirusbased shRNA constructs targeting wild-type EGFR mRNA can promote cell death. 2-ME2 structure More over, a decrease in cell viability was seen in EGFR wild type cells by Yamanaka et al. who examined the result of an EGFR siRNA, in various group of lung adenocarcinoma cell lines harboring a spectral range of EGFR wild-type, mutant, and KRAS mutant cell lines. Some differences were observed, although all cell lines examined in our study were painful and sensitive to your EGFR siRNA. Firstly, the differential sensitivity towards inhibition of cell development versus apoptosis induction wasn’t the same. The impact of an siRNA upon crucial aspects of the malignant phenotype, cell growth, and survival is a measure of the unique amplitude of the quality and efficiency of the different versions. The H1650 and HCC827 cell lines with the exon 19 removal were the most delicate, both for growth inhibition and apoptosis induction, confirming the exon 19 mutation could be the most oncogenic and addictive. H1650 cells have been called resistant to TKIs due the loss of a functional PTEN suppressor.