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目的:检测SOX2在胃癌组织中的表达,探讨SOX2对胃癌干细胞自我更新、增殖和转移能力的影响。方法:采用免疫组化检测SOX2在胃癌及癌旁组织中的表达情况。通过肿瘤球形成实验富集、分离胃癌干细胞。构建SOX2过表达慢病毒并感染胃癌干细胞中,通过实时定量PCR和western bolt检测感染慢病毒后胃癌干细胞中SOX2表达情况。分别利用肿瘤球形成实验检测SOX2对胃癌肿瘤干细胞自我更新能力的影响,CCK-8实验检测SOX2对胃癌干细胞增殖能力的影响,流式细胞术分析SOX2对胃癌干细胞的细胞周期的影响,Transwell实验检测SOX2对胃癌干细胞转移能力的影响。结果:SOX2在胃癌组织中表达显著低于癌旁组织。肿瘤球形成实验能够有效富集胃癌细胞SGC-7901和BGC-823的干细胞。慢病毒载体感染能够显著增强SOX2在胃癌干细胞中的表达。过表达SOX2能够抑制胃癌干细胞的自我更新、增殖和侵袭能力。结论:SOX2在胃癌中发挥抑癌基因的功能,其机制可能通过抑制肿瘤干细胞的自我更新、增殖和侵袭转移能力而抑制胃癌的发生发展。
Objective: To detect the expression of SOX2 in gastric cancer and to explore the effect of SOX2 on the self-renewal, proliferation and metastasis of gastric cancer stem cells. Methods: The expression of SOX2 in gastric cancer and its adjacent tissues was detected by immunohistochemistry. Enrichment and separation of gastric cancer stem cells by tumor ball formation experiments. SOX2 overexpression lentivirus was constructed and infected in gastric cancer stem cells. SOX2 expression in gastric cancer stem cells was detected by real-time quantitative PCR and western blot. The effect of SOX2 on the ability of self-renewal of gastric cancer stem cells was detected by the formation of tumor spheres. The effect of SOX2 on the proliferation of gastric cancer stem cells was examined by CCK-8 assay. The effect of SOX2 on the cell cycle of gastric cancer stem cells was analyzed by flow cytometry. Effects of SOX2 on metastasis of gastric cancer stem cells. Results: The expression of SOX2 in gastric cancer tissues was significantly lower than that in paracancerous tissues. Tumor formation assay effectively enriched the stem cells of gastric cancer cells SGC-7901 and BGC-823. Lentiviral vector infection can significantly enhance the expression of SOX2 in gastric cancer stem cells. Overexpression of SOX2 inhibits the ability of gastric cancer stem cells to self-renew, proliferate and invade. CONCLUSIONS: SOX2 plays a role of tumor suppressor gene in gastric cancer, and its mechanism may inhibit the occurrence and development of gastric cancer by inhibiting the self-renewal, proliferation and invasion and metastasis of cancer stem cells.