Objective：To preliminarily screen out the drug resistance-related genes downstream of signal transducer and activator of transcription 3 (STAT3) in human pancreatic cancer cell by small interfering RNA (siRNA) and gene chip technique, with the purpose of providing a basis for studying the mechanism of STAT3-associated drug resistance.
Methods：The differentially expressed genes between the human pancreatic SW1990 cells of wild-type STAT3 gene and STAT3 gene silenced by siRNA were compared after using gene chip technique to preliminarily screen out the drug resistance-related genes downstream of STAT3.
Results： Nine hundred and eighty-two (2.55%) differentially expressed genes were screened from the 47000 genes represented on the microarray according to the criterion of significant difference, of which, 592 genes were up-regulated by 2-fold and 390 genes were down-regulated by 2-fold, respectively. Among those, some drug resistance-related genes were identified that included significantly up-regulated genes of topoisomerase IIα (TOPOIIα) and TNF-related apoptosis-inducing ligand (TRAIL), and significantly down-regulated genes of cysteine-rich 61 (CYR61), RAS-related protein Rap-1A (RAP1A), BCL-2-associated athanogene 1 (BAG1) and cystic fibrosis transmembrane conductance regulator (CFTR).
Conclusions：The drug resistance of pancreatic cancer is a result of the interactions which involving multigenes and multipathways. The expression profile of six drug resistance-related genes changes after the STAT3 gene silencing with siRNA technique. Our results may provide new clues to further inspect the relation between STAT3 and drug resistance of pancreatic cancer, and also provide new insights into the treatment of pancreatic cancer.