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Background  Kirsten rat sarcoma ( KRAS)  mutations are widespread in lung adenocarcinoma patients. The combined utilization of  KRAS  antisense oligodeoxynucleotide ( ASODN ) and insulin‐like growth factor‐ I  receptor ( IGF‐IR ) may inhibit the proliferation of  A549  cell lines of lung adenocarcinoma.    Methods  Point mutations of the  KRAS  gene in  A549  cells were detected by polymerase chain reaction with special sequence primers ( PCR‐SSP ) and gene sequence analysis;  ASODN  was designed and synthesized according to the mutation specialty of  KRAS ; and the correlation of gene mutations and clinicopathological features were analyzed. Inhibition on the proliferation and morphostructure change were measured by methyl thiazolyl tetrazolium and colony‐forming unit assays. Flow cytometry was used to evaluate the expression of  KRAS  and  IGF‐IR  proteins and cell apoptosis and reverse transcriptase‐polymerase chain reaction were used to detect the expression of  KRAS  and  IGF‐IR  messenger ribonucleic acid ( mRNA) . Male nude mice were used to form the mice‐human lung cancer model and show the inhibition of  KRAS ASODN  on  A549  cells.    Results   PCR‐SSP  and gene sequence analysis results showed that the codon 12 of  KRAS  had changed from  GGT  to  GTT .  KRAS ASODN  or  IGF‐IR ASODN  could inhibit cell proliferation and promote apoptosis of  A549  cells. However, the combined utilization of  KRAS ASODN  and  IGF‐IR ASODN  could inhibit cell proliferation and promote apoptosis more powerfully than exclusive use of  KRAS ASODN  or  IGF‐IR ASODN .    Conclusion  The two  ASODNs  can inhibit the proliferation of lung adenocarcinoma cells through decreasing the expression of  KRAS  and  IGF‐IR mRNA  and protein.

thoracic cancer

Inhibition of lung adenocarcinoma cells by insulin‐like growth factor‐ I  receptor and  K irsten rat sarcoma mutations: A mutation analysis with antisense oligodeoxynucleotide