Renal cell carcinoma is the most common cancer of the kidney, and resistant to traditional therapies. The aim of this study is to investigate the effects of hydroxyapatite nanoparticles on human renal cell carcinoma 786-0 cells. Cell proliferation was assessed with an 3-(4,5-dimethylthiazol-2-yl) 2,5-diphenyltetrazolium bromide(MTT) staining kit. The apoptosis assay was assessed with an FITC Annexin V Apoptosis Detection Kit. Caspase-3 and caspase-12 were detected by immunocytochemical staining and semi-quantitative RT-PCR. Cell wound healing assay was used to ensure cell motility. Matrigel invasion assay was analysed via transwell chambers. Our results showed that hydroxyapatite nanoparticles significantly reduced cell proliferation, invasion and induced apoptosis of 786-0 cells. The inhibiting action may have relation with up-regulated caspase-12, leading the cells to apoptosis. This study suggests that hydroxyapatite nanoparticles may be an effective and delivery system for renal cell carcinoma therapy.
The effect and mechanism of phenylacetic acid on the proliferation of pancreatic carcinoma cells were investigated in cultured pancreatic carcinoma BXPC-3 cells by means of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and flow cytometry assay.The results show that the treatment of pancreatic carcinoma cells with phenylacetic acid significantly inhibited the cell proliferation in time-dependent and dose-dependent manners.The proliferation of BXPC-3 cells was inhibited at the stage of S phase,the cells at the end stage of S phase were accumulated abundantly,and thus DNA synthesis could not be accomplished entirely.In addition,the expression of adenosine deaminases acting on RNA(ADARs) mRNA in BXPC-3 cells and pancreatic carcinoma specimen were detected by RT-PCR.Having been treated with phenylacetic acid,ADAR2 mRNA in BXPC-3 cells was significantly decreased,the differences were of statistical significance(P<0.01).Taken together,these results suggest that phenylacetic acid may likely regulate the proliferation of pancreatic carcinoma cells through the regulation of ADAR2 mRNA expression.
