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AIM:To observe the effect of octreotide on apoptosis rateof human pancreatic cancer cells PC-3 after transfectedwith somatostatin receptor type 2(SST2)gene.METHODS:SST2 plasmid was transfected into PC-3 cellsby liposome.Result of transfection was detected byimmunocytochemical staining and Western blotting.Apoptosis rates of PC-3 cells under different dosages ofoctreotide were measured by MTT assay and flowcytometry(FCM).RESULTS:Apoptosis rate caused by octreotide oftransfected PO3 cells was 7.56+1.06% at the dosage of0.20μg/mL,9.25+1.73% at the dosage of 0.40μg/mL and14,18±2.71% at the dosage of 0.80μg/mL.Apoptosis ratecaused by octreotide of non-transfected PO3 cells was5.76+0.75% at the dosage of 0.20μg/mL,6,694.0.80% atthe dosage of 0.40μg/mL and 7.26+1.28% at the dosageof 0.80μg/mL.Transfected PC-3 cells growth inhibitionrate caused by octreotide was 9.36±1.34% at the dosageof 0.20μg/mL,12.03±1.44% at the dosage of 0.40μg/mLand 20.23±4.21% at the dosage of 0.80μg/mL.Non-transfected PC-3 cells growth inhibition rate caused byoctreotide was 6.44±0.66% at the dosage of 0.20μg/mL,7.65±0.88% at the dosage of 0.40μg/mL and 9.29±1.32%at the dosage of 0.80μg/mL.We found that octreotidecaused higher apoptosis rate and inhibition rate intransfected groups than in non-transfected groups(P<0.05)at the tested dosages(0.20,0.40 and 0.80μg/mL).CONCLUSION:Deficiency of SST2 was probably the majorreason why octreotide had little effect on PC-3 cells.Transfecting SST2 gene could strengthen the ability ofoctreotide of killing PC-3 cells.It provided an experimentalevidence for using both octreotide and transfection withSST2 gene on clinical treatment of pancreatic cancer.
AIM: To observe the effect of octreotide on apoptosis rate of human pancreatic cancer cells PC-3 after transfected with somatostatin receptor type 2 (SST2) gene. METHODS: SST2 plasmid was transfected into PC-3 cellsby liposome. Result of transfection was detected byimmunocytochemical staining and Apoptosis rates of PC-3 cells under different dosages of octreotide were measured by MTT assay and flowcytometry (FCM) .RESULTS: Apoptosis rate caused by octreotide of transfected PO3 cells was 7.56 + 1.06% at the dosage of 0.20 μg / mL, 9.25 + 1.73% at the dosage of 0.40 μg / mL and 14, 18 ± 2.71% at the dosage of 0.80 μg / mL.Apoptosis ratecaused by octreotide of non-transfected PO3 cells was 5.76 + 0.75% at the dosage of 0.20 μg / mL , 6,694.0.80% atthe dosage of 0.40 μg / mL and 7.26 + 1.28% at the dosage of 0.80 μg / mL. Transfected PC-3 cells growth inhibition rate caused by octreotide was 9.36 ± 1.34% at the dosageof 0.20 μg / mL, 12.03 ± 1.44% at the dosage of 0.40 μg / mL and 20.23 ± 4.21% at the dosage of 0.80 μg / mL.No n-transfected PC-3 cells growth inhibition rate caused byoctreotide was 6.44 ± 0.66% at the dosage of 0.20 μg / mL, 7.65 ± 0.88% at the dosage of 0.40 μg / mL and 9.29 ± 1.32% at the dosage of 0.80 μg / mL. We found that octreotidecaused higher apoptosis rate and inhibition rate intransfected groups than in non-transfected groups (P <0.05) at the tested dosages (0.20,0.40 and 0.80 μg / mL) .CONCLUSION: Deficiency of SST2 was probably the major reason why Transforming SST2 gene could strengthen the ability of octreotide of killing PC-3 cells. Provided an experimentalevidence for using both octreotide and transfection with SST2 gene on clinical treatment of pancreatic cancer.