半乳糖凝集素3在宫颈癌转移中的作用

目的检测宫颈癌样本中半乳糖凝集素3（Gal-3）的表达水平,研究其在宫颈癌转移中的作用。方法选取2009年6月1日至2010年6月1日于广州市第一人民医院妇产科诊治的宫颈癌患者为研究对象。癌组织活体取材,结合病理切片及临床诊断,将患者分为正常宫颈组织组（n=8）,原位癌（CINⅢ）组（n=12）,鳞癌I期组（n=10）,鳞癌Ⅱ期组（n=9）。所取标本分别为正常对照宫颈组织和不同临床分期的宫颈癌组织标本。免疫印迹法检测Gal-3蛋白的表达情况。体外培养宫颈癌细胞株HeLa及SiHa细胞,转染siRNA（50nmol/L）抑制Gal-3表达后,采用MTT法、Transwell侵袭小室法观察其对宫颈癌细胞株增殖和侵袭的影响。结果随着宫颈癌临床分期升高,Gal-3蛋白表达水平随之增加,与正常宫颈组织组比较,CIN、鳞癌I期（S（I））、鳞癌Ⅱ期（S（Ⅱ））组Gal-3蛋白分别增加了（35.2±8.4）%、（97.6±18.2）%和（179.4±20.7）%,差异均有统计学意义（P〈0.05）。在培养的宫颈癌HeLa、SiHa细胞株上,与转染对照siRNA比较,转染Gal-3siRNA48h后可明显抑制Gal-3蛋白表达,抑制率分别为（81.6±4.7）%、（87.5±6.8）%。转染特异性siRNA48h后,以普通培养液（含10%胎牛血清）继续培养细胞24h,与对照组（转染非特异性siRNA组）比较,HeLa及SiHa细胞增殖率分别降低（42.4±6.4）%、（50.6±7.2）%,差异均有统计学意义（P〈0.01）,侵袭细胞数目分别降低（48.6±5.8）%、（52.4±8.3）%,差异均有统计学意义（P〈0.01）。结论 Gal-3蛋白表达与宫颈癌临床分期密切相关,Gal-3可能通过促宫颈癌增殖和侵袭能力,促进宫颈癌的恶性进展。

Galectin 3 promotes cervical cancer metastasis

Objective To investigate the role of galectin 3 （Gal-3） in cervical cancer metastasis. Methods Cervical cancer samples in different clinical stages were taken from patients and the expression level of Gal-3 was examined by Western blot. Cervical cancer HeLa and SiHa cells were cultured. After transfection with specific Gal-3 siRNA, the proliferative rate and invasion number of cultured ceils were calculated by 3-（4,5-dimethylthiazol-2-yl）-2,5- diphenyhetrazolium bromide （MTF） assay and transwell chamber assay, respectively. Results The expression level of Gal-3 from sample tissues was gradually increased in parallel with the malignant progression of cervical cancer. In cultured cervical cancer HeLa and SiHa cells, transfection with specific Gal-3 siRNA （50 nmol/L） for 48 h largely inhibited Gal-3 protein expression, with the inhibitory rate of （81.6±4.7） % and （87.5±6.8） %, respectively. Compared with control group transfected with scrambled siRNA, transfection with Gal-3 siRNA resulted in deerease in prolierative rate, with the inhibitory rate of （42.4±6.4）% in HeLa ceils （n=4,P〈0.01） and （50.6±7.2）% in SiHa cells （n=4,P〈 0.01 ）. Moreover, the number of invasion cells was also decreased in cells transfected with Gal-3 siRNA, with the inhibitory rate of （48.6±5.8）% in HeLa cells （n=4, P〈0.01） and （52.4±8.3）% in SiHa cells （n=4,P〈0.01）. Conclusions The expression level of Gal-3 protein is tightly relative to cervical cancer clinical stage. Gal-3 promotes cervical cancer cell proliferation and invasion, which may contribute to cervical cancer malignant progression.