2002PubMedRequires access

[Antisense inhibition of cyclooxygenase-2 reduces malignant phenotype of gastric cancer cells].

Hanping Wu, Kaichun Wu, Liping Yao, Meihong Xu, Daiming Fan

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Abstract

OBJECTIVE: To investigate the role of cyclooxygenase-2 (COX-2) in tumorigenesis of gastric cancer, and the introduction of into human gastric cancer cells to suppress COX-2 expression. METHODS: The high COX-2 expressing human gastric cancer cell line SGC 7901 was stably transfected with the COX-2 antisense recombinant vector and plain vector (named as 7901-AS and 7901-P cells). The COX-2 expression levels in transfected cells were detected by immunocytochemistry and dot blotting methods. Proliferation and tumorigenic ability of transfected (7901-AS, 7901-P) and control (SGC 7901) cells were evaluated in vitro with MTT assay and in vivo with nude mice. RESULTS: Antisense treatment for COX-2 gene significantly reduced the expression level of COX-2 protein and mRNA and led inhibition of proliferation in 7901-AS cells. The tumor graft of 7901-AS in nude mice 30 days after implantation had less volume and weight than that of SGC7901 and 7901-P [(486.67 +/- 15.28) mg vs (826.67 +/- 77.67) mg and (776.67 +/- 300.06) mg, P < 0.01]. CONCLUSIONS: Overexpression of COX-2 in human gastric cancer cell line SGC 7901 was related to the malignant phenotype of cancer cells. Inhibition of COX-2 expression by antisense technique could reverse malignant phenotypes of gastric cancer cells.

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OBJECTIVE: To investigate the role of cyclooxygenase-2 (COX-2) in tumorigenesis of gastric cancer, and the introduction of into human gastric cancer cells to suppress COX-2 expression. METHODS: The high COX-2 expressing human gastric cancer cell line SGC 7901 was stably transfected with the COX-2 antisense recombinant vector and plain vector (named as 7901-AS and 7901-P cells). The COX-2 expression levels in transfected cells were detected by immunocytochemistry and dot blotting methods. Proliferation and tumorigenic ability of transfected (7901-AS, 7901-P) and control (SGC 7901) cells were evaluated in vitro with MTT assay and in vivo with nude mice. RESULTS: Antisense treatment for COX-2 gene significantly reduced the expression level of COX-2 protein and mRNA and led inhibition of proliferation in 7901-AS cells. The tumor graft of 7901-AS in nude mice 30 days after implantation had less volume and weight than that of SGC7901 and 7901-P [(486.67 +/- 15.28) mg vs (826.67 +/- 77.67) mg and (776.67 +/- 300.06) mg, P < 0.01]. CONCLUSIONS: Overexpression of COX-2 in human gastric cancer cell line SGC 7901 was related to the malignant phenotype of cancer cells. Inhibition of COX-2 expression by antisense technique could reverse malignant phenotypes of gastric cancer cells.

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Available abstract

OBJECTIVE: To investigate the role of cyclooxygenase-2 (COX-2) in tumorigenesis of gastric cancer, and the introduction of into human gastric cancer cells to suppress COX-2 expression. METHODS: The high COX-2 expressing human gastric cancer cell line SGC 7901 was stably transfected with the COX-2 antisense recombinant vector and plain vector (named as 7901-AS and 7901-P cells). The COX-2 expression levels in transfected cells were detected by immunocytochemistry and dot blotting methods. Proliferation and tumorigenic ability of transfected (7901-AS, 7901-P) and control (SGC 7901) cells were evaluated in vitro with MTT assay and in vivo with nude mice. RESULTS: Antisense treatment for COX-2 gene significantly reduced the expression level of COX-2 protein and mRNA and led inhibition of proliferation in 7901-AS cells. The tumor graft of 7901-AS in nude mice 30 days after implantation had less volume and weight than that of SGC7901 and 7901-P [(486.67 +/- 15.28) mg vs (826.67 +/- 77.67) mg and (776.67 +/- 300.06) mg, P < 0.01]. CONCLUSIONS: Overexpression of COX-2 in human gastric cancer cell line SGC 7901 was related to the malignant phenotype of cancer cells. Inhibition of COX-2 expression by antisense technique could reverse malignant phenotypes of gastric cancer cells.

Key concepts: Transfection, Carcinogenesis, Cancer, Cancer cell, Cell culture, Medicine, Molecular biology, Immunocytochemistry

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