[Corrigendum) RNA interference­mediated FANCF silencing sensitizes OVCAR3 ovarian cancer cells to adriamycin through increased adriamycin­induced apoptosis dependent on JNK activation.

After the publication of the article, an interested reader drew to the authors' attention that there appeared to be a pair of overlapping data panels in Fig. 4C on p. 1726 [specifically, the 'Untransfected' and 'Control shRNA' data panels for the ADM (24 h) experiments]. The authors have consulted their original data, and have realized that this figure was inadvertently assembled incorrectly. Furthermore, they have noticed that Fig. 1 on p. 1724 also contained errors that arose during its assembly; essentially, several of the data panels in Fig. 1C, showing the detection of FANCD2 focus formation via immunofluorescence experiments, were selected inappropriately. The corrected versions of Figs. 1 and 4, containing the corrected data panels for Figs. 1C and 4C respectively, are shown on the next page. Note that these errors did not affect the results or the conclusions reported in this work. The authors all agree to this Corrigendum, and are grateful to the Editor of Oncology Reports for allowing them to have the opportunity to correct these mistakes. Lastly, the authors apologize to the readership for any inconvenience these errors may have caused. [Oncology Reports 29: 1721­1729, 2013; DOI: 10.3892/or.2013.2295].

Safety, Pharmacokinetics, and Pharmacodynamics of a Dipeptidyl Peptidase-4 Inhibitor: A Randomized, Double-Blinded, Placebo-Controlled Daily Administration of Fotagliptin Benzoate for 14 Days for Type 2 Diabetes Mellitus.

This study investigated the pharmacokinetics, pharmacodynamics, and safety of fotagliptin benzoate (fotagliptin), a dipeptidyl peptidase-4 (DPP-4) inhibitor, in Chinese patients with type 2 diabetes mellitus (T2DM). In a randomized, double-blinded, placebo-controlled study, 10 and 4 patients with T2DM were randomized and received, respectively, once-daily oral fotagliptin (24 mg) or placebo, for 14 days. The pharmacokinetics and pharmacodynamics were assessed throughout the study, including monitoring DPP-4, glucagon-like peptide-1 (GLP-1), glycosylated hemoglobin, and fasting blood glucose. Fotagliptin was rapidly absorbed, and the median time to maximum concentration value was ∼1.5 hours. Plasma fotagliptin levels were stable after 14 days of once-daily dosage. The accumulation ratios for the area under the plasma concentration-time curve of fotagliptin, M1, and M2-1, were 1.19 ± 0.10, 1.59 ± 0.27, and 1.39 ± 0.26, respectively. The durations for DPP-4 inhibition >80% in the fotagliptin group on days 1 and 14 were 23.5 and 24.0 hours, respectively. The concentrations of GLP-1 were higher on days 1 and 14 than at the baseline. No serious complications occurred. Fotagliptin showed favorable pharmacokinetics and pharmacodynamics and was well tolerated. Treatment with fotagliptin can achieve high DPP-4 inhibition and increase plasma GLP-1. A once-per-day dosing regimen may be recommended as clinically efficacious.

RNA interference-mediated FANCF silencing sensitizes OVCAR3 ovarian cancer cells to adriamycin through increased adriamycin-induced apoptosis dependent on JNK activation.

In the present study, we downregulated FANCF expression by small interfering RNA (siRNA) in OVCAR ovarian cancer cells to address the effects of decreased FANCF expression on the function of the Fanconi anemia (FA)/breast cancer susceptibility gene (BRCA) pathway. Furthermore, we investigated whether this method increases the sensitivity of OVCAR3 cells to adriamycin (ADM) and the possible mechanism(s). We found that silencing of FANCF inactivated the FA/BRCA pathway by decreasing the monoubiquitination and focus formation of FANCD2 and reduced the function of the FA/BRCA pathway, resulting in the inhibition of cell proliferation, increased cell apoptosis and DNA damage in OVCAR3 cells. Moreover, we observed that silencing of FANCF enhanced the antiproliferative effect of ADM in OVCAR3 cells and increased ADM intracellular accumulation consequently sensitizing OVCAR3 cells to ADM. Furthermore, silencing of FANCF increased cell apoptosis of OVCAR3 cells which was caused by decreased mitochondrial membrane potential (MMP)-induced DNA damage, activated Jun N-terminal kinase (JNK), increased release of cytochrome c, increased expression of cleaved caspase-3 and poly(ADP-ribose) polymerase (PARP) dependent on JNK activation following treatment of ADM. Collectively, we confirm that silencing of FANCF sensitizes OVCAR3 ovarian cancer cells to ADM, suggesting that FANCF may serve as a potential target for therapeutic strategies in the treatment of ovarian cancer.

[Effect of troxerutin and cerebroproptein hydrolysate injection on platelet aggregation and thrombosis].

This study was purposed to explore the effect of troxerotin and cerebroproptein hydrolysate injection (TCHI) on platelet aggregation in vitro and thrombosis in vivo. The inhibitory rate of TCHI at different concentrations on platelet aggregation was determined by platelet aggregometer. The relationship between dose and effect was established. The effect of troxerutin and cerebroproptein hydrolysate injection on thrombosis was determined by the carotid thrombosis model of rats. The results showed that the TCHI could inhibit thrombosis and platelet aggregation in a concentration-dependent way. When the concentration of TCHI total nitrogen was 5 µg/ml, the inhibition rate of platelet aggregation reached to the highest value of 28.61 ± 22.07%, which is 2.5 times as much as that with 100 µg/ml aspirin. It is concluded that the TCHI has antiaggregative and antithrombotic activity effects against platelet aggregation and thrombosis.