We conclude that T. vaginalis may increase IL-1β expression in human prostate epithelium through activation of ROS, ERK, and NF-κB, and this in turn may induce the migration of neutrophils and monocytes and lead to an inflammatory response. This research is the first attempt to confirm inflammatory reaction caused by T. vaginalis in prostate epithelial cell.
The aim of the present study was to investigate the anti-cancer effects of the natural plant flavonoid, taxifolin, on human osteosarcoma cancer cells. Taxifolin was demonstrated to exhibit anti‑cancer effects on U2OS and Saos‑2 osteosarcoma cell lines. Treatment of cells with taxifolin inhibited proliferation and diminished colony formation in soft agar in a dose‑dependent manner. In vivo, intraperitoneal administration of taxifolin in nude mice bearing U2OS xenograft tumors, significantly inhibited tumor growth. In addition, taxifolin treatment was demonstrated to promote G1 cell cycle arrest and cell apoptosis in U2OS and Saos‑2 cell lines, as demonstrated by flow cytometry analysis. Western blot analysis demonstrated that taxifolin treatment was associated with a reduction in the expression levels of AKT serine/threonine kinase 1 (AKT), phosphorylated (p‑Ser473) AKT, v‑myc avian myelocytomatosis viral oncogene homolog (c‑myc) and S‑phase kinase associated protein 2 (SKP‑2) in U2OS and Saos‑2 cell lines. Overexpression of AKT considerably reversed the taxifolin‑induced decrease in AKT, c‑myc and SKP‑2 protein expression and the decrease in AKT phosphorylation, suggesting that inactivation of AKT was a mediator of taxifolin‑induced inhibition of c‑myc and SKP‑2. Furthermore, overexpression of SKP‑2 in U2OS cells partially reversed the growth inhibition mediated by taxifolin. Finally, taxifolin treatment repressed cell migration and invasion in U2OS cells and this effect was markedly reversed by SKP‑2 overexpression. The results of the present study indicate that taxifolin may present a potential novel therapeutic agent for osteosarcoma treatment.
Abstract. NY-ESO-1 belongs to the cancer testis antigens (CTA) family, and is identified in a variety of tumors. Certain studies have demonstrated that NY-ESO-1 predicts tumor recurrence and treatment response. No reports are currently available regarding the correlation between NY-ESO-1 and the recurrence of hepatocellular carcinoma (HCC) following surgery. The purpose of the present study was to evaluate the association between NY-ESO-1 and relapse of HCC and to explore the possible mechanisms for this correlation. A total of 120 HCC patients were analyzed for the expression of NY-ESO-1 by immunohistochemistry (IHC). A stable NY-ESO-1 over-expressed HepG2 cell line (ESO-HepG2) was established to determine the biological effects of NY-ESO-1 on cell proliferation, cell cycle and migration by using the xCELLigence DP system, flow cytometry and xCELLigence SP system. NY-ESO-1 was positive in 28 of 120 (23.3%) HCC tumor tissues. NY-ESO-1 was not detectable in adjacent normal liver tissues. A close correlation was found between NY-ESO-1 expression and the recurrence of HCC following surgery (P= 0.007). Kaplan-Meier analysis showed a shorter recurrence-free survival (RFS) for patients positive for NY-ESO-1 (log-rank test, P=0.003). The Cox regression model demonstrated that NY-ESO-1 expression was a significant independent predictor for the recurrence of HCC following curative surgery (P= 0.022). Compared with HepG2 cells, ESO-HepG2 cells have increased migration but not proliferation ability. In conclusion, NY-ESO-1 expression is associated with worse HCC outcome following surgery, and the mechanism for this finding may be that NY-ESO-1 increases tumor cell migration. IntroductionHepatocellular carcinoma (HCC) is the fifth most common cancer in the world and one of the most prevalent malignancies in Asia (1). Current curative treatment options include surgical resection and liver transplantation. Liver transplantation is effective only in the early stages of disease. Surgery is possible in few patients and curative in only a small percentage, due to recurrence following the surgery (2). Besides exploring effective therapeutic methods, investigators are attempting to find biomarkers to predict tumor recurrence. The NY-ESO-1 antigen was originally found in esophageal cancer by serological recombinant cDNA expression cloning (SEREX) and belongs to the cancer/testis antigen (CTA) family (3). NY-ESO-1 expression is restricted to testicular germ cells in normal adult tissues and is found in numerous malignancies including malignant melanoma, hepatoma, breast and lung cancer. The NY-ESO-1 protein is known to be markedly immunogenic for numerous advanced and metastatic types of cancer (4,5). NY-ESO-1 is a potential biomarker for the prediction of tumor recurrence and treatment outcomes in a variety of tumors, including gastrointestinal stromal tumors (6) and cutaneous melanoma (7).Although a number of studies showed inconsistently that NY-ESO-1 is positive in certain HCCs (8-16), two studies have demonstrated that NY-ESO-1 ...
The purpose of this study was to analyze the clinical characteristics of chronic hepatitis B (CHB) cured by antiviral therapy. Methods: Forty-two patients with CHB were enrolled. All patients had been treated with peginterferon (Peg-IFN) in combination with nucleoside analogue (NA) therapy for variable amounts of time, and all had been successfully cured of the disease. Results: The combined treatment time for all participants was 124.7 AE 58.8 weeks, and the average Peg-IFN treatment time was 102.6 AE 56.1 weeks. At 24 weeks, Hepatitis B surface antigen (HBsAg) and Hepatitis B e antigen (HBeAg) had decreased more than 50% from baseline. Multivariate logistic regression analysis of the week 96 HBsAg-clearing group and the non-HBsAg-clearing group showed a statistically significant difference in baseline HBV DNA levels and week 48 HBsAg levels. Those which baseline HBV DNA was < 2.75 log 10 IU/mL, and week 48 HBsAg levels were < 0.88 log 10 IU/mL were more likely to achieve rapid HBsAg clearance at 96 weeks. This suggests that low levels of baseline HBV DNA and week 48 HBsAg are a predictor of rapid HBsAg clearance at 96 weeks. Conclusions: Individualized extension of combination therapy to more than 96 weeks depending on the patient's response and adverse reaction conditions can help achieve a clinical cure. Patients with low baseline HBV DNA and low HBsAg levels at 48 weeks achieve HBsAg clearance more quickly than other populations.
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