CAJ | 학술논문

目的检测雄激素受体(AR)在乳腺癌细胞中的表达,并观察雄激素刺激对乳腺癌细胞增殖的影响.方法选择雌激素受体(ER)阳性的MCF-7和ER阴性的MDA-MB-453乳腺癌细胞,体外培养,Western blot技术检测两乳腺癌细胞株中AR蛋白的表达,MTT法检测用1×10-7、1×10-8和1×10-9 mol/L不同浓度的雄激素二氢睾酮(DHT)分别干预48、96、144 h后的细胞增殖,并应用流式细胞术检测DHT刺激乳腺癌细胞72 h后细胞周期的变化.结果两个乳腺癌细胞株经DHT作用后AR蛋白表达均增多,DHT通过AR抑制MCF-7和MDA-MB-453两个乳腺癌细胞株的生长,各时间段不同浓度组比较A值差异无统计学意义(P＞0.05),细胞周期结果显示G1期细胞比例增高,S期细胞比例降低.结论雄激素受体途径对ER阳性的MCF-7和ER阴性的MDA-MB-453乳腺癌细胞均有抑制生长作用,可能通过抑制细胞由G1期到S期转化来实现的.
목적 검측웅격소수체(AR)재유선암세포중적표체,병관찰웅격소자격대유선암세포증식적영향.방법 선택자격소수체(ER)양성적MCF-7화ER음성적MDA-MB-453유선암세포,체외배양,Western blot기술검측량유선암세포주중AR단백적표체,MTT법검측용1×10-7、1×10-8화1×10-9 mol/L불동농도적웅격소이경고동(DHT)분별간예48、96、144 h후적세포증식,병응용류식세포술검측DHT자격유선암세포72 h후세포주기적변화.결과 량개유선암세포주경DHT작용후AR단백표체균증다,DHT통과AR억제MCF-7화MDA-MB-453량개유선암세포주적생장,각시간단불동농도조비교A치차이무통계학의의(P＞0.05),세포주기결과현시G1기세포비례증고,S기세포비례강저.결론 웅격소수체도경대ER양성적MCF-7화ER음성적MDA-MB-453유선암세포균유억제생장작용,가능통과억제세포유G1기도S기전화래실현적.
Objective To evaluate the expression of androgen receptor (AR) in the breast cancer cell lines and its effect on proliferation of breast cancer cells. Methods The estrogen receptor (ER) -positive MCF-7 and ER-negative MDA-MB-453 cells were involved in this study and cultured in vitro. The expression of AR was detected by using Western blotting. Cell proliferation was determined by methyl thiazol tetrazolium (MTT) assay after the treatment with different concentrations of dihydrotestosterone (DHT) ( 1 x 10 -7, 1 x 10- 8, 1 x 10 -9 mol/L) for 48, 96 and 144 h respectively. Cell cycle was analyzed by flow cytometry following culture for 72 h. Results DHT increased the AR expression in the two breast cancer cell lines. AR pathway could inhibit proliferation of MCF-7 and MDA-MB-453 cells. There was no significant difference in absorbance values among three treatment groups at different time points (P ＞ 0. 05). Cell cycle analysis revealed that the proportion of cells at G1 phase was increased, and that at S phase decreased. Conclusion AR pathway may inhibit proliferation of ER-negative MDA-MB-453 breast cells as well as ER-positive MCF-7 cells, by suppressing the process of G1 to S phase progression.