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MiR-223-3p targets ECT2 to regulate cell cycle and apoptosis in gastric cancer cells

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Author:
No author available
Journal Title:
World Chinese Journal of Digestology
Issue:
2
DOI:
10.11569/wcjd.v26.i2.71
Key Word:
胃癌;上皮细胞转化序列2基因;miR-223-3p;细胞周期;凋亡;Gastric cancer;ECT2;MiR-223-3p;Cell cycle;Apoptosis

Abstract´╝Ü AIM To explore the role of miRNA-223-3p and epithelial cell transforming sequence 2 oncogene (ECT2) in cell cycle and apoptosis of gastric cancer (GC) cells and to analyze their correlation with clinicopathological characteristics.METHODS The expression of ECT2 and miR-223-3p in normal gastric mucosa cells (GSE-1) and GC cells (SGC-7901 and BGC-823) was detected by real-time fluorescent quantitative PCR and Western blot.Immunohistochemistry and RT-PCR were used to examine the expression of ECT2 and miR-223-3p in GC tissues and paired adjacent normal tissues,respectively.The correlation between ECT2 and miR-223-3p expression and clinicopathological characteristics was then analyzed.After miRNA-223-3p inhibitor and mimic were used to transfect SGC-7901 cells with LipofectamineTM2000,the expression of miRNA-223-3p and ECT2 was assessed by RT-PCR and Western blot in SGC-7901 cells.After another 24 h culture,the apoptosis rate and cell cycle progression were examined by flow cytometry.RESULTS The expression levels of ECT2 and miR-223-3p in GC cells were significantly increased as compared with those in normal gastric mucosa cells (P < 0.05 for both).In comparison with tumor adjacent normal tissues,the expression of ECT2 and miR-223-3p in GC tissues was significantly higher (P < 0.05).The expression of ECT2 and miR-223-3p was related to histologic differentiation (P < 0.05),Lauren type (P < 0.05),and TNM stage (P < 0.01),but not with gender,age,Bormann type,or tumor size (P > 0.05).Transfection with miR-223-3p mimic up-regulated ECT2 expression,whereas transfection of miR-223-3p inhibitor downregulated the expression of ECT2.Compared with negative control cells,the apoptosis rate of SGC-7901 cells transfected with miR-223-3p inhibitor significantly increased (P < 0.05),and the percentage of G1 phase cells also significantly increased in miR-223-3p inhibitor transfected cells (P < 0.05).CONCLUSION MiR-223-3p is closely related with cell cycle and apoptosis of gastric cancer cells,and it can regulate the occurrence and development of GC by influencing the expression of ECT2.ECT2 and miR-223-3p may serve as good factors to indicate the biologic behavior of GC.

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