[Lutein inhibits the adhesion, invasiveness and metastasis of human prostate cancer PC-3M cells].

OBJECTIVE: To explore the effects of lutein on the adhesion, invasiveness and metastasis of human prostate cancer PC-3M cells and its action mechanism. METHODS: We divided human prostate cancer PC-3M cells into a control, a low-dose lutein, a medium-dose lutein and a high-dose lutein group, and treated them with 0, 10, 20 and 40 µmol/L lutein, respectively. Then we examined the adhesion of the cells to matrix by cell adhesion assay and the changes in cell pseudopodia by Phalloidin staining, detected the expressions of paxillin, matrix metalloproteinase 2 (MMP-2), MMP-9, recombinant tissue inhibitors of metalloproteinase 1 (TIMP-1), E-cadherin, N-cadherin and vimentin by Western blot, determined the invasiveness and migration of the cells by scratch and Transwell assays, and observed their dynamic movement by high-intension imaging. RESULTS: Compared with the control, the lutein intervention groups showed significant reduction in the number of the cells adhered to matrix, the number of cell pseudopodia, the expressions of paxillin, MMP-2, MMP-9, N-cadherin and vimentin, the rates of migration, invasion and metastasis, and the distances of displacement and movement of the cells. However, the expressions of TIMP-1 and epithelial-mesenchymal transition-related E-cadherin were upregulated significantly. CONCLUSION: Lutein can inhibit cell adhesion, reduce the expressions of MMPs, and suppress cell invasion and migration by inhibiting the process of epithelial-mesenchymal transition.

Viromic analysis of feces from laboratory rabbits reveals a new Circovirus.

BACKGROUND: Members of the genus Circovirus with the family Circoviridae are responsible for fatal diseases that can affect mammals and birds. Beak and feather disease virus (BFDV) is responsible for fatal diseases that could affect birds, causing the psittacine beak and feather disease. The current study discovered a new Circovirus from feces of laboratory rabbits and name it RabCV, which shows close relationship to BFDVs. RESULTS: We investigated the feces virome of 10 laboratory rabbits using the viral metagenomic method. In these samples, we detected a new rabbit-associated Circovirus (RabCV) and performed phylogenetic analysis based on replication-associated (Rep) protein. The result showed that the RabCV was closely clustered with BFDVs, sharing the identity of 56.7%-57.2% with them based on the whole genome sequence. PCR screening in a cohort of 38 laboratory rabbits showed that 3 out of the 38 rabbits were positive for this new rabbit-associated Circovirus. CONCLUSION: A new Circovirus was discovered from feces of rabbits, which showed low prevalence in the healthy laboratory rabbits. BFDV is responsible for fatal diseases that could affect birds, which suggested that the potential threat of the new rabbit-associated Circovirus to the health of laboratory rabbits needs further study.

[Prostate cancer cell line PC-3 conditioned medium promotes proliferation and osteogenic differentiation of human bone marrow mesenchymal stem cells].

OBJECTIVE: To investigate the effects of prostate cancer cell line PC-3 conditioned medium (PC- 3-CM) on the proliferation and osteogenic differentiation of human bone marrow human basalis mesenchymal stem cells (hBMSCs). METHODS: hBMSCs were isolated and culture-expanded by density gradient centrifugation from normal volunteers. PC-3 cells were cultured till the time of logarithmic growth and then transferred to a fresh medium, which, after 24 hours of incubation, was collected as PC-3-CM. Passage 3 hBMSCs were cultured in the fresh medium alone (the control group) or that with 50% PC-3-CM (the experimental group), and the effect of PC-3-CM on the proliferation activity of the hBMSCs was detected by WST-8 assay. Based on the types of medium used, the hBMSCs were divided into Groups I (control), II (50% PC-3-CM), III (osteoblast inducer) and IV (osteoblast inducer containing 50% PC-3 CM). The effects of PC-3-CM on the osteoblastic differentiation of the hBMSCs were determined by ALP staining, ALP activity detection, Von Kossa staining, and calcium quantitation. RESULTS: At 1, 3, 5 and 7 days of incubation, the absorbance values of the cells in the experimental group were 0.4370 +/- 0.0285, 0.7980 +/- 0.0213, 1.9090 +/- 0.0612 and 2.3023 +/- 0.0610, and those in the control group were 0.4060 +/- 0.0223, 0.6643 +/- 0.0075, 1.3727 +/- 0.0176 and 1.7947 +/- 0.0115, respectively, with significant differences between the two groups (P < 0.01) except on day 1 (P > 0.05). The positive rate and intensity of ALP staining were gradually increased in the four groups, with the ALP activities of 0.29 +/- 0.03, 1.30 +/- 0.03, 2.13 +/- 0.08, and 3.80 +/- 0.03, respectively (P < 0.01), and so was the intensity of Von Kossa staining, with the calcium depositions of 0.04 +/- 0.01, 0.44 +/- 0.05, 0.98 +/- 0.03, and 1.27 +/- 0.04, respectively (P < 0.01). CONCLUSION: PC-3- CM can promote the proliferation and osteogenic differentiation of human bone marrow mesenchymal stem cells.

Neoadjuvant hormonal deprivation for patients undergoing radical prostatectomy.

The purpose of this study is to evaluate the therapeutic effect of radical prostatectomy combined with preoperative neoadjuvant hormonal ablation therapy for prostate cancer (PCa). In this study, a total of 31 patients with local PCa underwent radical prostatectomy; of these, 12 patients underwent preoperative hormonal deprivation with a combination of goserelin and flutamide for a period of 5.6 months. Data regarding clinical characteristics were compared between the neoadjuvant therapy and radical prostatectomy groups. A total of 31 patients received pelvic lymph node clearance, and the rate of positive lymph nodes was 12.9% (4/31). Serum prostate-specific antigen (PSA) was 8.9 +/- 1.2 microg L(-1) after the neoadjuvant therapy and 0.4 +/- 0.3 microg L(-1) one month after the radical prostatectomy. There were significant differences in the positive surgical margins, seminal vesicle invasion and lymph node metastasis between the neoadjuvant therapy group (n = 12) and the radical prostatectomy group (n = 19, P < 0.01). The resulsts indicates that preoperative hormonal deprivation induced by goserelin and flutamide can decrease clinical and pathological staging, but assessment of its influence on long-term prognosis requires further study.

Androgens induce increases in intracellular calcium via a G protein-coupled receptor in LNCaP prostate cancer cells.

The receptor mechanism of testosterone-induced nongenomic Ca2+ signaling in prostate cancer cells is poorly understood. In this study we investigated androgen-induced intracellular Ca2+ increases in LNCaP human prostate cancer cells with Fura-2 as a Ca2+ probe. 5alpha-dihydrotestosterone (DHT) produced fast and transient increases in intracellular Ca2+ in LNCaP cells in a concentration-dependent manner. These effects were abolished by extracellular Ca2+ removal or pretreatment with L-type Ca2+ channel inhibitors (nifedipine, verapamil, and diltiazem). Pretreatment with endoplasmic reticulum ryanodine receptor blocker (procaine) or phospholipase C inhibitor (neomycin sulfate) did not alter DHT-induced Ca2+ influx. The concentration of Ca2+ was also increased by impermeable testosterone conjugated to bovine serum albumin. Neither an antagonist of intracellular androgen receptors (cyproterone acetate) nor a protein synthesis inhibitor (cycloheximide) affected this fast Ca2+ influx. Furthermore, the effect of DHT was abolished in cells incubated with a G protein inhibitor (pertussis toxin) and a nonhydrolyzable analog of guanosine triphosphate (guanosine 5-[beta-thio]disphosphate) but not in cells incubated with the tyrosine kinase inhibitor genistein. These results indicate that androgens induced an L-type calcium channel-dependent intracellular Ca2+ increase in LNCaP prostate cancer cells. The rapid responses triggered by DHT did not appear to be mediated through classic intracellular androgen receptors, c-Src kinase-androgen receptor complex, or sex hormone-binding globulin but through a G protein-coupled receptor in LNCaP prostate cancer cells. These results may provide a new explanation for progression of prostate cancer.