中华肿瘤杂志
中華腫瘤雜誌
중화종류잡지
CHINESE JOURNAL OF ONCOLOGY
2013年
2期
89-93
,共5页
曾维根%胡攀%王佳妮%刘仁斌
曾維根%鬍攀%王佳妮%劉仁斌
증유근%호반%왕가니%류인빈
全反式维甲酸%乳腺肿瘤%肿瘤干细胞%细胞分化
全反式維甲痠%乳腺腫瘤%腫瘤榦細胞%細胞分化
전반식유갑산%유선종류%종류간세포%세포분화
All-trans retinoic acid%Breast neoplasms%Tumor stem cells%Cell differentiation
目的 研究全反式维甲酸(ATRA)对乳腺癌干细胞的抑制作用.方法 采用CCK-8法检测ATRA对MCF-7和SK-BR-3细胞及其干细胞的抑制作用,并检测ATRA处理前后干细胞表型CD44+ CD24-的比例变化.利用球囊形成实验,研究ATRA对乳腺癌干细胞的自我更新能力的影响;将球囊贴壁培养,观察ATRA对干细胞分化的影响.结果 ATRA能够有效的抑制MCF-7和SK-BR-3细胞及其干细胞,但干细胞对ATRA更加敏感.10-6 mol/L ATRA对MCF-7细胞和干细胞的抑制率分别为(8.66±1.06)％和(21.09±3.25)％ (P =0.004),对SK-BR-3细胞和干细胞的抑制率分别为(39.19 ±1.47)％和(51.22±2.80)％ (P =0.005).ATRA能有效地抑制干细胞的成球能力,破坏其自我更新能力.10-6 mol/L ATRA处理后,MCF-7和SK-BR-3干细胞成球率分别为5.2％ (5/96)和13.5％ (13/96),而对照组分别为86.5％(83/96)和93.8％(90/96,均P＜0.001).ATRA能促进CD44+ CD24-表型分化.10-6mol/L ATRA处理SK-BR-3干细胞后,CD44+ CD24-比例下降为(48.10±2.50)％,而对照组为(86.60±2.50)％ (P ＜0.001).结论 ATRA能有效地抑制乳腺癌细胞和干细胞,但是对干细胞更敏感;ATRA能破坏乳腺癌干细胞的自我更新能力,并促进其分化.
目的 研究全反式維甲痠(ATRA)對乳腺癌榦細胞的抑製作用.方法 採用CCK-8法檢測ATRA對MCF-7和SK-BR-3細胞及其榦細胞的抑製作用,併檢測ATRA處理前後榦細胞錶型CD44+ CD24-的比例變化.利用毬囊形成實驗,研究ATRA對乳腺癌榦細胞的自我更新能力的影響;將毬囊貼壁培養,觀察ATRA對榦細胞分化的影響.結果 ATRA能夠有效的抑製MCF-7和SK-BR-3細胞及其榦細胞,但榦細胞對ATRA更加敏感.10-6 mol/L ATRA對MCF-7細胞和榦細胞的抑製率分彆為(8.66±1.06)％和(21.09±3.25)％ (P =0.004),對SK-BR-3細胞和榦細胞的抑製率分彆為(39.19 ±1.47)％和(51.22±2.80)％ (P =0.005).ATRA能有效地抑製榦細胞的成毬能力,破壞其自我更新能力.10-6 mol/L ATRA處理後,MCF-7和SK-BR-3榦細胞成毬率分彆為5.2％ (5/96)和13.5％ (13/96),而對照組分彆為86.5％(83/96)和93.8％(90/96,均P＜0.001).ATRA能促進CD44+ CD24-錶型分化.10-6mol/L ATRA處理SK-BR-3榦細胞後,CD44+ CD24-比例下降為(48.10±2.50)％,而對照組為(86.60±2.50)％ (P ＜0.001).結論 ATRA能有效地抑製乳腺癌細胞和榦細胞,但是對榦細胞更敏感;ATRA能破壞乳腺癌榦細胞的自我更新能力,併促進其分化.
목적 연구전반식유갑산(ATRA)대유선암간세포적억제작용.방법 채용CCK-8법검측ATRA대MCF-7화SK-BR-3세포급기간세포적억제작용,병검측ATRA처리전후간세포표형CD44+ CD24-적비례변화.이용구낭형성실험,연구ATRA대유선암간세포적자아경신능력적영향;장구낭첩벽배양,관찰ATRA대간세포분화적영향.결과 ATRA능구유효적억제MCF-7화SK-BR-3세포급기간세포,단간세포대ATRA경가민감.10-6 mol/L ATRA대MCF-7세포화간세포적억제솔분별위(8.66±1.06)％화(21.09±3.25)％ (P =0.004),대SK-BR-3세포화간세포적억제솔분별위(39.19 ±1.47)％화(51.22±2.80)％ (P =0.005).ATRA능유효지억제간세포적성구능력,파배기자아경신능력.10-6 mol/L ATRA처리후,MCF-7화SK-BR-3간세포성구솔분별위5.2％ (5/96)화13.5％ (13/96),이대조조분별위86.5％(83/96)화93.8％(90/96,균P＜0.001).ATRA능촉진CD44+ CD24-표형분화.10-6mol/L ATRA처리SK-BR-3간세포후,CD44+ CD24-비례하강위(48.10±2.50)％,이대조조위(86.60±2.50)％ (P ＜0.001).결론 ATRA능유효지억제유선암세포화간세포,단시대간세포경민감;ATRA능파배유선암간세포적자아경신능력,병촉진기분화.
Objective To detect the inhibitory effect of all-trans retinoic acid (ATRA) on breast cancer stem cells (CSCs).Methods The inhibitory effect of ATRA on MCF-7 and SK-BR-3 cell lines was analyzed using a Cell Counting Kit-8 (CCK-8).The proportion of CD44 + CD24-tumor cells of the two cell lines were measured before and after the ATRA treatment,and the role of ATRA in the regulation of CSC self-renewing ability was evaluated with a tumor sphere assay.The tumor spheres were grown in an adherent culture to evaluate the ATRA-induced differentiation of breast cancer stem cells.Results ATRA effectively inhibited the unsorted cells and stem cells,but the CSCs were more sensitive to ATRA.At a concentration of 10-6 mol/L,the inhibitory rate of MCF-7 unsorted cells and stem cells were (8.66 ± 1.06) ％ and (21.09 ±3.25)％,respectively (P =0.004).For SK-BR-3 cells,the rates were (39.19 ± 1.47)％ and (51.22 ±2.80)％,respectively (P =0.005).The self-renewing ability of the CSCs was impaired by ATRA at a concentration of 10-6 mol/L.The rate of MCF-7 and SK-BR-3 stem cells to form tumor sphere was 5.2％ (5/96) and 13.5％ (13/96),respectively.For the control group,it was 86.5％ (83/96) and 93.8％ (90/96),respectively (P ＜ 0.001).ATRA also promoted the CD44 + CD24-subpopulation to differentiate.SK-BR-3 stem cells were grown in an adherent culture.After using ATRA,the proportion of CD44 + CD24-cells was (48.1±2.5)％ and that of the control groupwas (86.6±2.5)％ (P＜0.001).Conclusions ATRA effectively inhibits breast NCSCs and CSCs,but CSCs are more sensitive to ATRA.ATRA impairs the selfrenewing ability of CSCs and promotes CSCs to differentiate.
