中国肿瘤临床
中國腫瘤臨床
중국종류림상
CHINESE JOURNAL OF CLINICAL ONCOLOGY
2013年
8期
431-435
,共5页
郑旭%孙保存%赵秀兰%王进京%董学易%古强%孙冉
鄭旭%孫保存%趙秀蘭%王進京%董學易%古彊%孫冉
정욱%손보존%조수란%왕진경%동학역%고강%손염
血管生成拟态%上皮间充质转化%肺肉瘤样癌%免疫组织化学
血管生成擬態%上皮間充質轉化%肺肉瘤樣癌%免疫組織化學
혈관생성의태%상피간충질전화%폐육류양암%면역조직화학
vasculogenic mimicry%epithelial-to-mesenchymal transition%pulmonary sarcomatoid carcinoma%immunohistochemistry
目的:研究肺肉瘤样癌(pulmonary sarcomatoid carcinoma,PSC)中血管生成拟态(vasculogenic mimicry,VM)的临床意义,阐述上皮间充质转化(epithelial-to-mesenchymal transition,EMT)提高PSC的恶性度及促进VM形成的相关机制.方法:对肺肉瘤样癌组织切片22例进行HE、CD31和PAS双重染色,Twist、Vimentin、E-cadherin、VEGF免疫组织化学染色,分析VM相关的临床意义及EMT促进VM形成的相关机制.结果:22例中4例(18.2%)存在VM,Kaplan-Meier生存分析提示有无VM肿瘤患者比较生存时间差异有统计学意义(P<0.05).VM阳性患者Twist的阳性率较阴性患者高,且差异有统计学意义(P<0.05).Twist1的表达与VEGF、E-cadherin、Vimentin的表达存在明显相关性.结论:VM是患者预后的不利因素,肺肉瘤样癌中发生了EMT,转录因子Twist1可能通过下调E-cadherin,上调Vimentin诱导EMT,并可能通过上调VEGF的表达促进VM的形成,从而促进肿瘤的侵袭和转移.
目的:研究肺肉瘤樣癌(pulmonary sarcomatoid carcinoma,PSC)中血管生成擬態(vasculogenic mimicry,VM)的臨床意義,闡述上皮間充質轉化(epithelial-to-mesenchymal transition,EMT)提高PSC的噁性度及促進VM形成的相關機製.方法:對肺肉瘤樣癌組織切片22例進行HE、CD31和PAS雙重染色,Twist、Vimentin、E-cadherin、VEGF免疫組織化學染色,分析VM相關的臨床意義及EMT促進VM形成的相關機製.結果:22例中4例(18.2%)存在VM,Kaplan-Meier生存分析提示有無VM腫瘤患者比較生存時間差異有統計學意義(P<0.05).VM暘性患者Twist的暘性率較陰性患者高,且差異有統計學意義(P<0.05).Twist1的錶達與VEGF、E-cadherin、Vimentin的錶達存在明顯相關性.結論:VM是患者預後的不利因素,肺肉瘤樣癌中髮生瞭EMT,轉錄因子Twist1可能通過下調E-cadherin,上調Vimentin誘導EMT,併可能通過上調VEGF的錶達促進VM的形成,從而促進腫瘤的侵襲和轉移.
목적:연구폐육류양암(pulmonary sarcomatoid carcinoma,PSC)중혈관생성의태(vasculogenic mimicry,VM)적림상의의,천술상피간충질전화(epithelial-to-mesenchymal transition,EMT)제고PSC적악성도급촉진VM형성적상관궤제.방법:대폐육류양암조직절편22례진행HE、CD31화PAS쌍중염색,Twist、Vimentin、E-cadherin、VEGF면역조직화학염색,분석VM상관적림상의의급EMT촉진VM형성적상관궤제.결과:22례중4례(18.2%)존재VM,Kaplan-Meier생존분석제시유무VM종류환자비교생존시간차이유통계학의의(P<0.05).VM양성환자Twist적양성솔교음성환자고,차차이유통계학의의(P<0.05).Twist1적표체여VEGF、E-cadherin、Vimentin적표체존재명현상관성.결론:VM시환자예후적불리인소,폐육류양암중발생료EMT,전록인자Twist1가능통과하조E-cadherin,상조Vimentin유도EMT,병가능통과상조VEGF적표체촉진VM적형성,종이촉진종류적침습화전이.
Objective: The expression and clinical significance of vasculogenic mimicry (VM) were investigated. The related mechanisms of epithelial-to-mesenchymal transition (EMT) in VM formation and worsening of pulmonary sarcomatoid carcinoma (PSC) were examined. Methods:Hematoxylin and eosin staining, CD31/periodic acid-Schiff double staining, and immunohistochemi-cal staining were performed to determine the expression of VM, Twist1, vascular endothelial growth factor (VEGF), E-cadherin, and vi-mentin in the tissues of 22 PSC patients. The clinical significance of VM and the mechanism of EMT in VM formation were explored. Results:VM was found in four (18.2%) of the 22 PSC patients. Kaplan–Meier survival analysis revealed that the patients with VM had a shorter survival period than those without the VM expression, with statistically significant differences found between the two groups. Comparative results of the groups with and without VM expression showed a higher positive rate of Twist1 expression in the former group (P<0.05). Significant correlations were observed between the Twist1 expression and the VEGF, E-cadherin, and vimentin expression. Conclusion:VM unfavorably influences the prognosis of PSC patients. Twist1 can upregulate Vimentin and downregulate E-cadherin by inducing EMT. Additionally, it may upregulate VEGF to promote VM formation, which increases tumor invasions and metastases.