肿瘤影像学
腫瘤影像學
종류영상학
Oncoradiology
2014年
3期
200-204
,共5页
徐俊彦%郑宇佳%罗建民%张建平%章英剑%程竞仪%叶定伟
徐俊彥%鄭宇佳%囉建民%張建平%章英劍%程競儀%葉定偉
서준언%정우가%라건민%장건평%장영검%정경의%협정위
11C-乙酸%肾细胞癌%脂肪酸合酶
11C-乙痠%腎細胞癌%脂肪痠閤酶
11C-을산%신세포암%지방산합매
11C-acetate%Renal cell carcinoma%Fatty acid synthase
目的:11C-乙酸(11C-AC)PET/CT诊断肾细胞癌的灵敏度高于18F-脱氧葡萄糖(18F-FDG),但其显像机制尚不明确。本研究探讨其被肾细胞癌摄取是否与细胞膜脂肪酸合成相关。方法①细胞抑制实验:培养3株肾癌细胞(786-0、ACNH和Caki-1),分别以脂肪酸合酶(FAS)抑制剂C75、二甲基亚砜(DMSO)预处理后加入11C-AC,30 min后测细胞摄取放射性计数,并收集细胞提取液测定蛋白浓度,以蛋白免疫印迹检测FAS表达。②小动物PET/CT显像:对786-0荷瘤裸鼠行11C-AC显像,测得肿瘤与软组织的靶本比(T/B),处死裸鼠,取肿瘤组织,免疫组织化学检测FAS表达。结果786-0细胞株实验组比对照组摄取11C-AC量明显降低,每微克蛋白的放射性摄取值分别为2.430±0.107和3.544±0.443(P=0.013),降低率为31.42%。蛋白免疫印迹实验显示,实验组FAS表达明显低于对照组。ACNH和Caki-1细胞株实验组与对照组每微克蛋白的放射性摄取和FAS表达均无显著差异。小动物PET/CT显示,裸鼠皮下肿瘤11C-AC摄取明显增高,肿瘤免疫组织化学检测FAS表达强阳性。结论肾透明细胞癌原发灶的11C-AC摄取与FAS表达有关,但不同病理类型摄取乙酸的程度不同。
目的:11C-乙痠(11C-AC)PET/CT診斷腎細胞癌的靈敏度高于18F-脫氧葡萄糖(18F-FDG),但其顯像機製尚不明確。本研究探討其被腎細胞癌攝取是否與細胞膜脂肪痠閤成相關。方法①細胞抑製實驗:培養3株腎癌細胞(786-0、ACNH和Caki-1),分彆以脂肪痠閤酶(FAS)抑製劑C75、二甲基亞砜(DMSO)預處理後加入11C-AC,30 min後測細胞攝取放射性計數,併收集細胞提取液測定蛋白濃度,以蛋白免疫印跡檢測FAS錶達。②小動物PET/CT顯像:對786-0荷瘤裸鼠行11C-AC顯像,測得腫瘤與軟組織的靶本比(T/B),處死裸鼠,取腫瘤組織,免疫組織化學檢測FAS錶達。結果786-0細胞株實驗組比對照組攝取11C-AC量明顯降低,每微剋蛋白的放射性攝取值分彆為2.430±0.107和3.544±0.443(P=0.013),降低率為31.42%。蛋白免疫印跡實驗顯示,實驗組FAS錶達明顯低于對照組。ACNH和Caki-1細胞株實驗組與對照組每微剋蛋白的放射性攝取和FAS錶達均無顯著差異。小動物PET/CT顯示,裸鼠皮下腫瘤11C-AC攝取明顯增高,腫瘤免疫組織化學檢測FAS錶達彊暘性。結論腎透明細胞癌原髮竈的11C-AC攝取與FAS錶達有關,但不同病理類型攝取乙痠的程度不同。
목적:11C-을산(11C-AC)PET/CT진단신세포암적령민도고우18F-탈양포도당(18F-FDG),단기현상궤제상불명학。본연구탐토기피신세포암섭취시부여세포막지방산합성상관。방법①세포억제실험:배양3주신암세포(786-0、ACNH화Caki-1),분별이지방산합매(FAS)억제제C75、이갑기아풍(DMSO)예처리후가입11C-AC,30 min후측세포섭취방사성계수,병수집세포제취액측정단백농도,이단백면역인적검측FAS표체。②소동물PET/CT현상:대786-0하류라서행11C-AC현상,측득종류여연조직적파본비(T/B),처사라서,취종류조직,면역조직화학검측FAS표체。결과786-0세포주실험조비대조조섭취11C-AC량명현강저,매미극단백적방사성섭취치분별위2.430±0.107화3.544±0.443(P=0.013),강저솔위31.42%。단백면역인적실험현시,실험조FAS표체명현저우대조조。ACNH화Caki-1세포주실험조여대조조매미극단백적방사성섭취화FAS표체균무현저차이。소동물PET/CT현시,라서피하종류11C-AC섭취명현증고,종류면역조직화학검측FAS표체강양성。결론신투명세포암원발조적11C-AC섭취여FAS표체유관,단불동병리류형섭취을산적정도불동。
Objective The sensitivity of diagnosing renal cell carcinoma (RCC) by 11C-acetate (11C-AC) PET/CT is higher than 18F-fluorodeoxyglucose (18F-FDG). However, the mechanism of 11C-AC uptake in the tumor is not definite. The present paper aims to identify the correlation between 11C-AC uptake and fatty acid synthesis of cell membrane. Methods In vitro cell uptake and inhibition: 786-0, ACNH and Caki-1 (human renal carcinoma) were cultured, and then treated with C75 (a FAS inhibitor) and dimethyl sulfoxide (DMSO, as control). After 11C-AC was added to cells for 30 min, the lysis extracts were measured in a γ-counter and the protein contents were determined. Then, FAS expression was determined by Western blotting. Micro PET/CT: 786-0-bearing nude mice were scanned by 11C-AC PET/CT and tumor to soft tissue ratios were measured. After imaging, the mice were euthanized, and the tumors were excised for immunohistochemical analysis. Results The 786-0 cells treated with C75 showed inhibition uptake by 31.42% (P=0.013) compared with the control cells. There were no significant differences in 11C-AC uptake between treated cells and control cells for ACNH and Caki-1 cell lines. The visual inspection of the Western blotting results revealed significant differences in band intensity for 786-0 cells, but no differences were found in band intensity for the other two cell lines. The tumors showed significant uptake in micro PET/CT and strong positive in immunohistochemical analysis of FAS expression. Conclusion The 11C-AC uptake in the primary sites of renal clear cell carcinoma was related to the expression of FAS, but different pathological types of renal tumors may utilize acetate through other metabolic pathways.