中华皮肤科杂志
中華皮膚科雜誌
중화피부과잡지
Chinese Journal of Dermatology
2009年
12期
831-834
,共4页
黑色素瘤%细胞系%肿瘤%PPARγ%罗格列酮%基质金属蛋白酶2
黑色素瘤%細胞繫%腫瘤%PPARγ%囉格列酮%基質金屬蛋白酶2
흑색소류%세포계%종류%PPARγ%라격렬동%기질금속단백매2
Melanoma%Cell line,tumor%PPAR gamma%Rosiglitazone%Matrix metalloproteinase 2
目的 探讨过氧化物酶体增殖物激活受体-γ(PPAR-γ)配体罗格列酮对人黑素瘤细胞体外侵袭能力的影响及机制.方法 体外培养人黑素瘤细胞株A375;噻唑蓝法(MTT)检测罗格列酮对A375细胞的增殖抑制率;RT-PCR、Western印迹检测罗格列酮对黑素瘤侵袭相关基因基质金属蛋向酶2(MMP2)、组织金属蛋白酶抑制剂2(TIMP2)表达的影响.Matrigel侵袭实验检测罗格列酮对黑素瘤细胞体外侵袭能力的影响.结果 MTT结果显示,在24 h干预点,罗格列酮浓度为10、25μmol/L时,对A375细胞增殖抑制率分别为(4.86±0.31)%、(5.15±0.52)%,细胞毒性作用不明显.罗格列酮能在mRNA和蛋白水平下调MMP2的表达(P<0.01),并上调TIMP2 mRNA的表达(P<0.01).侵袭实验显示,对照组、10 μmol/L罗格列酮组、25 μmol/L罗格列酮组穿过Transwell小室膜的A375细胞数依次为210.7±14.9,154.1±7.7,87.3±8.1,差异有统计学意义(P<0.01).结论 罗格列酮能抑制人黑素瘤细胞株A375的转移,可能与其下调MMP2的表达有关.
目的 探討過氧化物酶體增殖物激活受體-γ(PPAR-γ)配體囉格列酮對人黑素瘤細胞體外侵襲能力的影響及機製.方法 體外培養人黑素瘤細胞株A375;噻唑藍法(MTT)檢測囉格列酮對A375細胞的增殖抑製率;RT-PCR、Western印跡檢測囉格列酮對黑素瘤侵襲相關基因基質金屬蛋嚮酶2(MMP2)、組織金屬蛋白酶抑製劑2(TIMP2)錶達的影響.Matrigel侵襲實驗檢測囉格列酮對黑素瘤細胞體外侵襲能力的影響.結果 MTT結果顯示,在24 h榦預點,囉格列酮濃度為10、25μmol/L時,對A375細胞增殖抑製率分彆為(4.86±0.31)%、(5.15±0.52)%,細胞毒性作用不明顯.囉格列酮能在mRNA和蛋白水平下調MMP2的錶達(P<0.01),併上調TIMP2 mRNA的錶達(P<0.01).侵襲實驗顯示,對照組、10 μmol/L囉格列酮組、25 μmol/L囉格列酮組穿過Transwell小室膜的A375細胞數依次為210.7±14.9,154.1±7.7,87.3±8.1,差異有統計學意義(P<0.01).結論 囉格列酮能抑製人黑素瘤細胞株A375的轉移,可能與其下調MMP2的錶達有關.
목적 탐토과양화물매체증식물격활수체-γ(PPAR-γ)배체라격렬동대인흑소류세포체외침습능력적영향급궤제.방법 체외배양인흑소류세포주A375;새서람법(MTT)검측라격렬동대A375세포적증식억제솔;RT-PCR、Western인적검측라격렬동대흑소류침습상관기인기질금속단향매2(MMP2)、조직금속단백매억제제2(TIMP2)표체적영향.Matrigel침습실험검측라격렬동대흑소류세포체외침습능력적영향.결과 MTT결과현시,재24 h간예점,라격렬동농도위10、25μmol/L시,대A375세포증식억제솔분별위(4.86±0.31)%、(5.15±0.52)%,세포독성작용불명현.라격렬동능재mRNA화단백수평하조MMP2적표체(P<0.01),병상조TIMP2 mRNA적표체(P<0.01).침습실험현시,대조조、10 μmol/L라격렬동조、25 μmol/L라격렬동조천과Transwell소실막적A375세포수의차위210.7±14.9,154.1±7.7,87.3±8.1,차이유통계학의의(P<0.01).결론 라격렬동능억제인흑소류세포주A375적전이,가능여기하조MMP2적표체유관.
Objective To explore the effect ofrosiglitazone (RGZ), a ligand of peroxisome proliferatoractivated receptor γ (PPARγ), on the invasiveness of A375 cells in vitro and its mechanism of action.Methods A375 human melanoma cells were cultured in vitro and treated with different concentrations of RGZ. The proliferation of the cells, mRNA expression levels of matrix metalloproteinase (MMP) 2 and tissue inhibitor of metalloproteinase (TIMP) 2, protein expression of MMP2 in A375 cells were detected by MTT assay, semi-quantitative RT-PCR and Western-blot, respectively. The invasiveness of A375 cells was detected by Matrigel invasion assay. Results MTT assay showed that the proliferation of A375 cells was inhibited by (4.86±0.31 )% and (5.15±0.52)% under the 24-hour treatment with RGZ of 10 and 25 μmol/L, respectively, and no evident cytotoxity was observed for RGZ. Compared with untreated A375 ceils, a significant decrease was observed in the mRNA and protein expression of MMP2 in A375 ceils treated with RGZ of 10 and 25 μmol/L (all P < 0.05), along with an increase in the mRNA expression of TIMP2 (both P < 0.01 ).The count of A375 cells transmigrating through matrigel was 154.1±7.7 and 87.3±8.1 under the treatment with RGZ of 10 and 25 μmol/L, significantly lower than that of those without treatment (210.7±14.9,both P < 0.01 ). Conclusions RGZ could inhibit the transmigration of A375 ceils, likely by down-regulating the mRNA and protein expression of MMP2.
