The aim of this study was to investigate the effects and mechanisms of baicalin against prostate cancer cell growth and cell cycle progression. A human prostate cancer cell line LNCaP was engrafted into nude mice, and the oncogenicity of LNCaP cells was analyzed. The 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT) assay was used to measure LNCaP and PC3 proliferation capability. CDK6 mRNA level was detected using qRT-PCR. Western blotting was performed to assess the levels of cell cycle-associated proteins. In addition, cell cycle and apoptosis were analyzed using flow cytometry. Baicalin significantly decreased the expression of cell cycle-associated proteins. Furthermore, baicalin showed an observable effect on proliferation, cell cycle progression and apoptosis in LNCaP and PC3 cells. Upregulation of CDK6 and FOXM1 reversed the effect of baicalin. CDK6- and FOXM1-mediated cell growth attenuated the protective effect of baicalin in prostate cancer. This study presented an understanding of the role and mechanism of baicalin in prostate cancer cells, providing a new target and therapies for the prevention and treatment of prostate cancer.

中文翻译：

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黄ical苷通过CDK6 / FOXM1轴抑制前列腺癌细胞的细胞周期进程和增殖。

这项研究的目的是研究黄ical苷对前列腺癌细胞的生长和细胞周期进程的影响和机制。将人前列腺癌细胞系LNCaP移植到裸鼠中，并分析LNCaP细胞的致癌性。使用3- [4,5-二甲基噻唑-2-基] -2,5-二苯基溴化四唑（MTT）测定LNCaP和PC3的增殖能力。使用qRT-PCR检测CDK6 mRNA水平。进行蛋白质印迹以评估细胞周期相关蛋白的水平。此外，使用流式细胞仪分析细胞周期和凋亡。黄ical苷显着降低细胞周期相关蛋白的表达。此外，黄ical苷对LNCaP和PC3细胞的增殖，细胞周期进程和细胞凋亡显示出可观察到的作用。CDK6和FOXM1的上调逆转了黄ical苷的作用。CDK6和FOXM1介导的细胞生长减弱了黄ical苷对前列腺癌的保护作用。这项研究提出了对黄ical苷在前列腺癌细胞中的作用和机制的理解，为预防和治疗前列腺癌提供了新的靶标和疗法。