IL-6调节miR-21在激素抵抗性前列腺癌中的机制研究

Research on the mechanism of IL-6 regulate miR-21 in the process of castration recurrent prostate carcinoma

目的检测转染微核糖核酸-21抑制剂(miR-21-inhibitor)前后前列腺癌细胞PC3在不同白细胞介素-6(IL-6)浓度下微核糖核酸-21(miR-21)的表达情况,细胞的增殖能力及雄激素受体(AR),转录信号诱导和激活者3(STAT3)水平。分析IL-6和miR-21在前列腺癌非依赖性进程中的作用及意义。方法通过RT-PCR检测不同IL-6浓度培养下非依赖性细胞系PC3在转染miR-21前后miR-21的表达情况。通过CCK-8检测转染前后细胞的增殖能力。通过western blot检测不同IL-6浓度培养下PC3细胞AR,STAT3的表达情况。结果转染miR-21能显著的抑制前列腺癌细胞miR-21的表达量,并抑制前列腺癌细胞的增殖。IL-6在短期促进PC3细胞的增殖,并且诱导miR-21的高表达。IL-6短期能够诱导PC3细胞系AR,STAT3高表达。结论 IL-6在非依赖性前列腺癌的进展中起重要作用,长期培养下IL-6对前列腺癌细胞系的作用需要进一步研究。miR-21与前列腺癌的恶性程度及依赖性相关,在前列腺癌的非依赖性进程中起重要作用,miR-21有希望成为非依赖性前列腺癌的一个潜在治疗靶点。IL-6可以诱导miR-21高表达,AR,STAT3在这一通路中起重要作用。

Objective To detect the different expression of microRNA-21 （miR-21）and androgen receptor（AR） , STAT3 and multiplication capacity between prostate carcinoma （Pca）cell line PC3 cultured in distinct concentration of interleukin-6 （ IL-6 ）before or after the infection and to investigate the function and significance of IL-6 and miR-21 in the Pca＇s process of androgen independent. Methods RT-PCR was used to detect the expression of miR-21 between prostate carcinoma cell line PC3 cultured in distinct concentration of IL-6 before or after the infection. CCK-8 was applied to check the cell line＇s multiplication capacity before or after the infection. Different expression of AR and STAT3 in the distinct concentration of interleukin-6 were detected by western blot. Results miR-21-inhibitor can significantly inhibit the expression of miR-21 in prostate cancer cell PC3, and inhibit the proliferation of prostate cells. IL - 6 promotes PC3 cell proliferation in the short term, and induces miR- 21 expression. IL-6 could induce AR and STAT3 high expression in PC3 cells. Conclusions IL-6 plays a critical role in the process of androgen independent cell lines. More study on androgen dependent cell lines is required, miR-21 is important in the process of androgen independent, miR-21-inhibitor is promising as a potential way to cure prostate cancer. IL-6 promotes miR-21 expression. AR and Stat3 play a critical role in this signal pathway.