Kiss-1抑制宫颈癌细胞增殖和侵袭的作用机制
Mechanism of Kiss-1 Inhibiting Proliferation and Invasion of Cervical Cancer Cells

目的：研究kiss-1基因在宫颈癌SiHa细胞增殖活力和侵袭迁徙能力中发挥的作用机制，以便为宫颈癌的治疗提供新的靶点。方法：选取kiss-1基因过表达后稳定转染SiHa宫颈癌细胞。本实验分为3组。1) 空白组为常规宫颈癌SiHa细胞；2) 空载体组为转染空载体的宫颈癌SiHa细胞；3) 过表达组为转染稳定kiss-1基因的宫颈癌SiHa细胞。Western blot法分析3组kiss-1基因蛋白的表达量差异，CCK-8测出3组细胞增殖活力，Transwell模型测3组细胞侵袭能力和转移能力。结果：过表达组kiss-1基因蛋白表达量最高，过表达组中Ecadherin的表达是明显上调(P < 0.05)，相反Vimentin的表达明显下调(P < 0.05)。转染kiss-1基因的过表达组细胞增殖活力明显低于其他两组(P < 0.05)，尤其在12小时的穿膜细胞个数计数方面，转染kiss-1基因过表达组的个数显著高于其他两组(P < 0.05)。转染kiss-1基因的过表达组可明显的抑制宫颈癌SiHa细胞的侵袭能力和转移能力。结论：kiss-1基因过表达能显著抑制宫颈癌疾病侵袭转移。
Objective: To study the mechanism of Kiss-1 in the proliferation and invasion of cervical cancer SiHa cell, and analyze the relative mechanism to supply effective therapy targets to cervical cancer. Methods: Kiss-1 over expression plasmid was transfected into cervical cancer cell lines of SiHa. There were three groups. 1) SiHa control; 2) Treated with empty vector; 3) Treated with kiss-1 gene vector. Western blot analysis of three groups kiss-1 gene protein expression, cell proliferation via-bility was measured by CCK-8, and cell invasion ability and metastasis ability in the transwell model. Results: After transfection of pEGFPC1/Kiss-1 into cervical cancer cell lines of SiHa (over-express group), the protein of kiss-1 was highest, the expression of E-cadherin was significantly higher (P < 0.05); however, the expression of Vimentin was significantly lower than other groups (P < 0.05). Migration ability of the cells in over-expression group was decreased than SiHa control (P < 0.05). The migrating cells were obviously decreased than SiHa control at 12 h after transfection of pEGFPC1/Kiss-1 into SiHa cells (P < 0.05). Over-express group of Kiss-1 could decrease the invasion ability and metastasis ability of cervical cancer SiHa. Conclusion: Over-express of Kiss-1 gene could decrease the potential of invasion and metastasis of cervical cancer.