Published online Aug 1, 2004. doi: 10.3748/wjg.v10.i15.2292
Revised: December 3, 2003
Accepted: December 16, 2003
Published online: August 1, 2004
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 cells by liposome. Result of transfection was detected by immunocytochemical staining and Western blotting. Apoptosis rates of PC-3 cells under different dosages of octreotide were measured by MTT assay and flow cytometry (FCM).
RESULTS: Apoptosis rate caused by octreotide of transfected PC-3 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 rate caused by octreotide of non -transfected PC-3 cells was 5.76 ± 0.75% at the dosage of 0.20 μg/mL, 6.69 ± 0.80% at the 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 dosage of 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. Non-transfected PC -3 cells growth inhibition rate caused by octreotide 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 octreotide caused higher apoptosis rate and inhibition rate in transfected 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 octreotide had little effect on PC-3 cells. Transfecting SST2 gene could strengthen the ability of octreotide of killing PC-3 cells. It provided an experimental evidence for using both octreotide and transfection with SST2 gene on clinical treatment of pancreatic cancer.