DNA vector-based Stat3-specific RNA interference （si-Stat3） blocks Stat3 signalling and inhibits prostate tumour growth. However, the antitumour activity depends on the efficient delivery of si-Stat3. The effects on the growth of mouse prostate cancer cells of si-Stat3 delivered by hydroxyapatite were determined in this study. RM-1 tumour blocks were transplanted into C57BIJ6 mice. CaCl2-modified hydroxyapatite carrying si-Stat3 plasmids were injected into tumours, and tumour growth and histology were determined. The expression levels of Star3, pTyr-Stat3, Bcl-2, Bax, Caspase3, VEGFand cyclin D1 were measured by western blot analysis. Amounts of apoptosis in cancer cells were analysed with immunohistochemistry and the terminal deoxyribonucleotidyl transferase-mediated dUTP-digoxigenin nick end-labelling （TUNEL） assay. The results showed that hydroxyapatite-delivered si-Stat3 significantly suppressed tumour growth up to 74% （P〈0.01）. Stat3 expression was dramatically downregulated in the tumours. The immunohistochemistry and TUNEL results showed that si-Stat3-induced apoptosis （up to 42%, P〈0.01）. The Stat3 downstream genes Bcl-2, VEGFand cyclin DI were also strongly downregulated in the tumour tissues that also displayed significant increases in Bax expression and Caspase3 activity. These results suggest that hydroxyapatite can be used for the in vivo delivery of plasmid-based siRNAs into tumours.
The potential association between xenotropic murine leukaemia virus-related gammaretrovirus （XMRV） and prostate cancer （PCa） has been documented since 2006, It is important for furthering our understanding of the biological mechanisms of PCa to ascertain whether this association is causal. To summarize the available information on the epidemiological and laboratory findings of the association, we conducted a literature search of the PubMed electronic database （from March 2006 to February 2011） to identify relevant published studies that examined the association between XMRV and PCa, Although several studies showed the positive association between XMRV and PCa, more recent studies did not support this conclusion, The positive findings might be due to contamination of human samples, Further studies are needed to clarify this association,
The aim of this study was to determine and examine the possible reasons for the difference in prostate cancer incidence between Asian men and North American men by literature review. Data regarding cancer incidence and mortality were obtained from the database of the International Agency for Research on Cancer （IARC）. A literature review was conducted by studying related articles published in peer-reviewed journals such as the The New England Journal of Medicine, Journal of Clinical Oncology, A Cancer Journal for Clinicians and Asian Journal of Andrology. To evaluate the early diagnosis and survival rates, the mortality.to-incidence rate ratio （MR/IR） was calculated from the IARC data. By comparing prostate cancer data between Asian men and North American men, we found that differences in the incidence rate and MR/IR could be attributed largely to a lack of annual prostate cancer screening with serum prostate-specific antigen （PSA） in most Asian countries. It is likely that PSA screening also contributes significantly to the differences in prostate cancer mortality rates. Prostate cancer has the highest incidence rate among five common malignancies in Asian Americans. However, the MR/IR ratio of prostate cancer is the lowest among cancers. These data seem to further support the usefulness of PSA screening, even though the percentage of low risk cancers is greater in prostate cancer than in other cancers. The low incidence rate of prostate cancer does not reflect the actual statistics of this disease in Asia. The data from limited institutions in many Asian countries seem to bias the true incidence and mortality rates. To improve this situation, incorporating PSA screening for prostate cancer, as well as constructing a nationwide cancer registration system, will be helpful.
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（P0.01）.Taken together,these results suggest that phenylacetic acid may likely regulate the proliferation of pancreatic carcinoma cells through the regulation of ADAR2 mRNA expression.
