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Background  Epidermal growth factor receptor‐ t yrosine kinase inhibitors ( TKI‐EGFRs)  present a new prospect for the treatment of lung cancer. However, in clinical application, the majority of patients become  TKI  resistant within a year. More and more studies have shown that a loss of phosphatase and tensin homolog ( PTEN)  expression is associated with  TKI  resistance. An alternative method of upregulating  PTEN  expression may reverse  TKI  resistance.    Methods  We designed five candidate small activating ribonucleic acids ( saRNA s) to target  PTEN , and transfected them into H‐157 cells to screen out functional  saRNA . We used reverse transcriptase‐polymerase chain reaction and Western blot to evaluate the effect of  saRNA  to  PTEN  expression. We then analyzed the growth and apoptosis of cells transfected with  saRNA  under the treatment of  TKI  to investigate whether  saRNAs  can reverse  TKI  resistance by upregulating  PTEN  expression.    Results  The functional  saRNA  we designed could upregulate  PTEN  expression. The H‐157 cells transfected with  saRNA  grew slower in the presence of TKI drugs than the cells that were not transfected with  saRNA . The apoptosis rate was also obviously higher.    Conclusions  Our study proves that loss of  PTEN  expression is an important mechanism of  TKI  resistance. It is possible to control  TKI  resistance by upregulating  PTEN  expression using RNA activation technology.

thoracic cancer

Small activating ribonucleic acid reverses tyrosine kinase inhibitor resistance in epidermal growth factor receptor‐mutant lung cancer by increasing the expression of phosphatase and tensin homolog