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AIM:To investigate the effect of transfected survivin antisenseoligonucleotide (ASODN) on proliferation and apoptosis ofgastric cancer ceils.METHODS:The authors designed ASODNs targetingdifferent regions of survMn mRNA,including survivingASODN1,ASODN2 and ASODN3.ASODNs were transfectedinto gastric cancer cell line SGC 7901,cell growth was detectedby MTT assay.Cells exposed to the potent oligonucleotidewere also examined for apoptosis induction by FCM andfluorescence microscopy.Semiquantitive RT-PCR andWestern blot examinations were carried for expression ofsurvivin mRNA and protein.RESULTS:ASODN3 caused a statistically significantreduction of cell viability to 60.6% (±2.9%) (P<0.01),whileASODN1 and ASODN2 had no such changes (P>0.05).Thecell growth was also significantly inhibited by ASODN3,compared with reversal and scrambled sequence.A significantloss of survivin mRNA was presented in ASODN3 treatedceils and this was not seen in treatment with sense ODNor scramble ODN.Protein level was significantly decreased48 h after survivin ASODN trasfected by approximately 2-folddecrease comparedwith untreated controls.However.ASODN3 did not induce significant apoptosis response until48 h after transfection (P>0.05).CONCLUSION:ASODN3,which targets translation initiationpart,can be identified as a most potent antisense compound.Srvivin ASODN3 may provide a novel approach to therapyof gastric cancer.
AIM: To investigate the effect of transfected survivin antisenseoligonucleotide (ASODN) on proliferation and apoptosis of gastric cancer cells. METHODS: The authors designed ASODNs targeting different regions of survMn mRNA, including surviving ASODN1, ASODN2 and ASODN3.ASODNs were transfected in gastric cancer cell line SGC 7901, cell growth was detected by MTT assay. Cells were exposed to the potent oligonucleotidewere also examined for apoptosis induction by FCM and fluorescence microscopy. Semiquantitive RT-PCR and Western blot examinations were carried for expression of survivin mRNA and protein .RESULTS: ASODN3 caused a significant significant of cell viability to While ASODN1 and ASODN2 had no such changes (P> 0.05). The cell growth was also significantly inhibited by ASODN3, compared with reversal and scrambled sequence. A significant loss of survivin mRNA was presented in 60.6% (± 2.9% ASODN3 treatedceils and this was not seen in treatment with sense ODNor scramble ODN.Protein level was significantly decreased 48 h after survivin ASODN trasfected by approximately 2-fold decrease compared with untreated controls. After null. ASODN 3 did not induce significant apoptosis response until 48 h after transfection (P> 0.05) .CONCLUSION: ASODN3, which targets translation initiationpart, can be identified as a most potent antisense compound. Srvivin ASODN3 may provide a novel approach to therapy of gastric cancer.