摘要
目的研究CCDC33在人小细胞肺癌中的表达、临床病理学意义及相应的作用机制。方法分析了138例人非小细胞肺癌中CCDC33蛋白表达和亚细胞定位与临床病理因素的关系,采用免疫组织化学染色,免疫印迹方法和Transwell法探讨其对非小细胞肺癌增殖、侵袭能力影响的机制。结果 CCDC33在肺癌组织的细胞浆中高表达,阳性率为57.9%(80/138),明显高于相对应的癌旁组织14.7%(10/68,<0.001),且其高表达与非小细胞肺癌的低分化(=0.006)、高TNM分期(=0.008)、淋巴结转移(=0.002)明显相关。干扰CCDC33活化的betacatenin表达下降,肺癌细胞的侵袭转移能力也明显下降。结论 CCDC33参与非小细胞肺癌的发生发展,促进侵袭和转移,与激活经典Wnt通路相关。
Objective To study the expression and clinical pathological significance of CCDC33 in human non-small cell lung cancer（NSCLC）. Methods Immunohistochemistry was performed to test the expression of CCDC33 in 138 cases non-small cell lung cancer（NSCLC）. Western blot and Transwell were used to examine the expression of CCDC33 and proliferation and invasion abilities of NSCLCs. Results CCDC33 was highly expressed in the cytoplasm of NSCLCs（57.9%, 80/149）, much more than the adjacent normal lung tissues（14.7%, 10/68,P〈 0.001）, and correlated with low differentiation（ P= 0.006）, high TNM staging（P =0.008）, lymph node metastasis（ P=0.002）. The CCDC33 knockdown by si RNA significantly downregulated the expression of beta-catenin,decreased the proliferation and invasion and metastasis of lung cancer cells. Conclusion CCDC33 might be involved in the pathogenesis of NSCLC and enhanced the invasion and metastasis via canonical Wnt signaling pathway.
出处
《解剖科学进展》
2015年第6期618-620,623,共4页
Progress of Anatomical Sciences
基金
教育部高等学校博士点基金(博导类
20132104110 025)
