Huang Yaqiang, Huang Hongxing, Han Zhaodong, Li Wei, Mai Zhipeng, Yuan Runqiang
Department of Urology, Zhongshan City People's Hospital, Zhongshan 528400, China.
Department of Urology, Guangzhou First People's Hospital, Guangzhou 510180, China.
J Nanosci Nanotechnol. 2019 Apr 1;19(4):1942-1950. doi: 10.1166/jnn.2019.16404.
To explore the molecular mechanism by which ginsenoside Rh2 (G-Rh2) inhibits prostate cancer by regulating vascular growth. Different concentrations of G-Rh2 with three prostate cancer cell lines (LNCaP, PC3 and DU145) were transplanted in nude mice, and tumor mass volume was measured over time. LNCaP, PC3 and DU145 were co-cultured with vascular endothelial cells to determine the optimal concentration of G-Rh2 by MTT assay. LNCaP, PC3 and DU145 were cultured under the selected concentration (0, 0.01, 0.05, 0.1, 0.5 and 1 mg/mL) of G-Rh2, and the expression levels of CD31, VEGF, PDGF and CNNM1 detected by qRT-PCR and western blot. The expression pattern of CD31 was detected in CNNM1 overexpressed and knockout LNCaP, PC3 and DU145 cells under G-Rh2. G-Rh2 significantly inhibited the growth of all three prostate cancer cell lines in the dorsum of nude mice ( <0.05), and the increment rate of vascular endothelial cells co-cultured with LNCaP, PC3 and DU145 ( <0.05). The expression of CD31, VEGF, PDGF and CNNM1 genes in LNCaP, PC3 and DU145 cells was inhibited by G-Rh2. Overexpression of CNNM1 reversed the inhibitory effect of G-Rh2 on the expression of CD31 in these cells ( <0.05), while the function of knockout of CNNM1 and the inhibitory effect of G-Rh2 appeared to be similar ( <0.05). In conclusion, G-Rh2 inhibited prostate cancer growth by inhibiting its angiogenesis through decreasing the expression of CNNM1 in the cancer cells.
探讨人参皂苷Rh2（G-Rh2）通过调节血管生成抑制前列腺癌的分子机制。将不同浓度的G-Rh2与三种前列腺癌细胞系（LNCaP、PC3和DU145）接种于裸鼠体内，随时间测量肿瘤体积。将LNCaP、PC3和DU145与血管内皮细胞共培养，通过MTT法确定G-Rh2的最佳浓度。将LNCaP、PC3和DU145在选定浓度（0、0.01、0.05、0.1、0.5和1mg/mL）的G-Rh2下培养，通过qRT-PCR和蛋白质印迹法检测CD31、VEGF、PDGF和CNNM1的表达水平。在G-Rh2作用下，检测CNNM1过表达和敲除的LNCaP、PC3和DU145细胞中CD31的表达模式。G-Rh2显著抑制裸鼠背部所有三种前列腺癌细胞系的生长（<0.05），以及与LNCaP、PC3和DU145共培养的血管内皮细胞的增殖率（<0.05）。G-Rh2抑制LNCaP、PC3和DU145细胞中CD31、VEGF、PDGF和CNNM1基因的表达。CNNM1的过表达逆转了G-Rh2对这些细胞中CD31表达的抑制作用（<0.05），而敲除CNNM1的作用与G-Rh2的抑制作用似乎相似（<0.05）。总之，G-Rh2通过降低癌细胞中CNNM1的表达抑制血管生成，从而抑制前列腺癌生长。
