中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2011年
10期
1623-1626
,共4页
崔越宏%吴伟忠%刘天舒%谢倩%刘康达
崔越宏%吳偉忠%劉天舒%謝倩%劉康達
최월굉%오위충%류천서%사천%류강체
癌,肝细胞%热休克蛋白%17AAG%增殖%侵袭
癌,肝細胞%熱休剋蛋白%17AAG%增殖%侵襲
암,간세포%열휴극단백%17AAG%증식%침습
Carcinoma,hepatocellular%Heat shock proteins%17AAG%Proliferation%Invasion
目的 观察17-丙烯胺基-17-去甲氧基格尔德霉素(17AAG)对肝癌细胞的增殖、侵袭和转移能力的抑制作用.方法 检测1μmol/L 17AAG对细胞增殖、侵袭能力和凋亡的影响,观察0.1 μmol/L和1.0μmol/L 17AAG对其靶点热休克蛋白(HSP) 90表达的影响.结果 17AAG对HL7702肝脏细胞无生长抑制作用,对肝母细胞瘤细胞HepG2[ 24、48和72 h IC50值分别为( 14182.94 ±6369.90)、(1.56±0.19)和(0.02±0.00) μmol/L]和肝癌细胞MHCC-97H[ 24、48和72 h IC50值分别为(5660.49±3029.33)、(3.30±0.31)和(1.55±0.12) μmol/L]均有生长抑制作用,影响细胞周期,降低其离散和侵袭的能力,并诱导凋亡,对裸鼠皮下移植瘤生长具有抑制作用,降低肿瘤的肺、肝转移.17AAG上调HSP90的表达.结论 17AAG对HepG2细胞和MHCC-97H细胞具有增殖抑制、诱导凋亡和降低转移能力的作用,而对HL-7702肝脏细胞则无生长抑制及诱导凋亡的作用.
目的 觀察17-丙烯胺基-17-去甲氧基格爾德黴素(17AAG)對肝癌細胞的增殖、侵襲和轉移能力的抑製作用.方法 檢測1μmol/L 17AAG對細胞增殖、侵襲能力和凋亡的影響,觀察0.1 μmol/L和1.0μmol/L 17AAG對其靶點熱休剋蛋白(HSP) 90錶達的影響.結果 17AAG對HL7702肝髒細胞無生長抑製作用,對肝母細胞瘤細胞HepG2[ 24、48和72 h IC50值分彆為( 14182.94 ±6369.90)、(1.56±0.19)和(0.02±0.00) μmol/L]和肝癌細胞MHCC-97H[ 24、48和72 h IC50值分彆為(5660.49±3029.33)、(3.30±0.31)和(1.55±0.12) μmol/L]均有生長抑製作用,影響細胞週期,降低其離散和侵襲的能力,併誘導凋亡,對裸鼠皮下移植瘤生長具有抑製作用,降低腫瘤的肺、肝轉移.17AAG上調HSP90的錶達.結論 17AAG對HepG2細胞和MHCC-97H細胞具有增殖抑製、誘導凋亡和降低轉移能力的作用,而對HL-7702肝髒細胞則無生長抑製及誘導凋亡的作用.
목적 관찰17-병희알기-17-거갑양기격이덕매소(17AAG)대간암세포적증식、침습화전이능력적억제작용.방법 검측1μmol/L 17AAG대세포증식、침습능력화조망적영향,관찰0.1 μmol/L화1.0μmol/L 17AAG대기파점열휴극단백(HSP) 90표체적영향.결과 17AAG대HL7702간장세포무생장억제작용,대간모세포류세포HepG2[ 24、48화72 h IC50치분별위( 14182.94 ±6369.90)、(1.56±0.19)화(0.02±0.00) μmol/L]화간암세포MHCC-97H[ 24、48화72 h IC50치분별위(5660.49±3029.33)、(3.30±0.31)화(1.55±0.12) μmol/L]균유생장억제작용,영향세포주기,강저기리산화침습적능력,병유도조망,대라서피하이식류생장구유억제작용,강저종류적폐、간전이.17AAG상조HSP90적표체.결론 17AAG대HepG2세포화MHCC-97H세포구유증식억제、유도조망화강저전이능력적작용,이대HL-7702간장세포칙무생장억제급유도조망적작용.
Objective To observe whether 17AAG can inhibit the proliferation,invasion and metastatic ability of hepatocellular carcinoma (HCC) cells.Methods The changes of proliferative and invasive abilities and apoptosis of HCC cells treated with 1 μmol/L 17AAG were tested.The change of HSP90 expression in HCC cells treated with 0.1 and 1.0 μmol/L 17AAG was detected by using Western blotting.Results There was no growth inhibition in HL7702 hepatocytes.17AAG could inhibit the growth of HepG2 cells [IC50 of 24,48 and72 h:(14182.94 ±6369.90),(1.56±0.19) and (0.02±0.00)μmol/L] and MHCC-97H cells [ IC50 of 24,48 and 72 h:(5660.49 ± 3029.33 ),(3.30 ± 0.31 ) and ( 1.55 ±0.12) μmol/L],and decrease the ability of scattering and invasion.17AAG also affected the cell cycle and induced apoptosis of HepG2 and MHCC-97H cells.17AAG inhibited the growth of transplanted tumors in nude mice and the metastasis of the lung and liver.The expression of HSP90 was elevated by 17AAG.Conclusion 17AAG inhibited the proliferation and metastatic ability of HepG2 and MHCC-97H cells,and induced apoptosis.However,there were no growth inhibition and apoptosis induction in HL7702 hepatocytes.
