Gastric Cancer
Copyright ©The Author(s) 2004. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Apr 15, 2004; 10(8): 1121-1124
Published online Apr 15, 2004. doi: 10.3748/wjg.v10.i8.1121
Survivin antisense oligodeoxynucleotide inhibits growth of gastric cancer cells
Jian-Hui Yang, Yi-Chu Zhang, Hui-Qing Qian
Jian-Hui Yang, Department of Oncological Surgery, Shidong Hospital, 200090, Shanghai, China
Yi-Chu Zhang, Department of General Surgery, Xinhua Hospital Affiliated to Shanghai Second Medical University, Shanghai 200092, China
Hui-Qing Qian, Department of Surgical Laboratory, Xinhua Hospital Affiliated to Shanghai Second Medical University, Shanghai 200092, China
Author contributions: All authors contributed equally to the work.
Supported by Shanghai Key Research Project Grant in Medical Science Development (99ZD003).
Correspondence to: Dr. Jian-Hui Yang, Department of Oncological Surgery, Shidong Hospital, Ningguo Road 236, Shanghai 20090, China. yangjianhuicn@sohu.com
Telephone: +86-21-65433031-3204 Fax: +86-21-65111710
Received: March 4, 2003
Revised: April 1, 2003
Accepted: April 9, 2003
Published online: April 15, 2004
Abstract

AIM: To investigate the effect of transfected survivin antisense oligonucleotide (ASODN) on proliferation and apoptosis of gastric cancer cells.

METHODS: The authors designed ASODNs targeting different regions of survivin mRNA, including surviving ASODN1, ASODN2 and ASODN3. ASODNs were transfected into gastric cancer cell line SGC 7901, cell growth was detected by MTT assay. Cells exposed to the potent oligonucleotide were 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 statistically significant reduction of cell viability to 60.6% (± 2.9%) (P < 0.01), 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 ASODN3 treated cells and this was not seen in treatment with sense ODN or scramble ODN. Protein level was significantly decreased 48 h after survivin ASODN trasfected by approximately 2-fold decrease compared with untreated controls. However, ASODN3 did not induce significant apoptosis response until 48 h after transfection (P > 0.05).

CONCLUSION: ASODN3, which targets translation initiation part, can be identified as a most potent antisense compound. Srvivin ASODN3 may provide a novel approach to therapy of gastric cancer.

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