Search

Introduction: This study aims to explore the relationship betweenextracellular histone and prostate cancer and its mechanism. Methods: Migration of prostate cancer cells was detected by Transwell. Inflammatory factor expression was investigated by ELISA. Epithelial-mesenchymal transition and expression of NF-κB pathway-related proteins were investigated using Western blotting. Results: Under the induction of extracellular histones, the migration rate of prostate cancer cells and the levels of IL-1β, TNF-α, and IL-6 were notably enhanced. Then, expression of E-cadherin was significantly down-regulated, while levels of N-cadherin, vimentin, β-catenin, Snail, p-p65 and p-IκBα were significantly up-regulated, which was reversed by PDTC (pyrrolidine dithiocarbamate). Conclusion: Extracellular histone significantly promotes the progression of prostate cancer cells via NF-κB pathway-mediated inflammatory responses, which may serve as a novel target for treating prostate cancer.

Increasing evidence indicates that inflammation plays a role in pig-to-baboon organ xenotransplantation. We have evaluated serum amyloid A (SAA) as a marker of inflammation in baboons with various pig xenografts. We measured SAA levels in recipient baboons with pig artery patch (n = 5), life-supporting kidney (n = 5), heterotopic heart (n = 2), or hepatocyte (n = 1) grafts and using an OmniChek-SAA for Inflammation & Infection kit. C-reactive protein (CRP), another marker of inflammation (e.g. D-dimer), was also measured.SAA indicated increased inflammation when baboons developed consumptive coagulopathy (CC; e.g. thrombocytopenia) or infection. SAA also indicated that treatment of the recipient with tocilizumab reduced inflammation. There was significant positive correlation between SAA with changes in CRP (r = 0.6, P

Dysfunction of microRNAs (miRs) has been implicated in the development and progression of various human cancers. Our previous study demonstrated that miR-101 inhibited bladder cancer cell proliferation and invasion through inhibition of c-FOS expression. As an miR generally has many targets, other targets of miR-101 may also serve important roles in bladder cancer progression. Reverse transcription-quantitative polymerase chain reaction and western blot analyses were used to examine mRNA and protein expression, respectively. Wound healing and Transwell assays were conducted to study cell migration and invasion, respectively. The luciferase reporter gene assay was performed to verify one of the targets of miR-101. The data in the present study indicate that the expression of miR-101 is significantly reduced in bladder cancer tissues compared with that in adjacent non-tumour tissues. In addition, miR-101 expression is also downregulated in bladder cancer cell lines compared with that in normal bladder epithelial cells. Furthermore, low expression of miR-101 was significantly associated with tumour metastasis, advanced clinical stage, and poor prognosis in bladder cancer. Frizzled class receptor 4 (FZD4) was identified as a novel target of miR-101 in bladder cancer cells. The expression of FZD4 was significantly upregulated in bladder cancer tissues and cell lines. Both miR-101 overexpression and FZD4 inhibition caused a significant reduction of the migration and invasion of bladder cancer cells, whereas overexpression of FZD4 reversed the suppressive effects of miR-101 on bladder cancer cell migration and invasion. In conclusion, it was demonstrated that miR-101 downregulation is associated with bladder cancer progression and that miR-101 can inhibit bladder cancer cell migration and invasion via directly targeting FZD4. The present study expands the understanding of the molecular mechanisms underlying bladder cancer progression.

MicroRNAs (miRs) have important roles in the parthenogenesis of malignancies. While it has been suggested that deregulation of miR‑101 is involved in bladder cancer, the underlying mechanisms have remained largely elusive. The present study aimed to investigate the roles of miR‑101 in the regulation of bladder cancer cell proliferation and invasion. Reverse‑transcription quantitative polymerase chain reaction analysis revealed that the expression of miR‑101 was significantly reduced in the HT‑1376, BIU87, T24 and 5637 several human bladder cancer cell lines compared to that in the SV‑HUC‑1 normal bladder epithelial cell line. Furthermore, a Targetscan search and a luciferase assay were used to identify c‑FOS as a novel target of miR‑101, and western blot analysis indicated that the protein expression of c‑FOS was shown to be negatively regulated by miR‑101 in bladder cancer T24 cells; however, c‑FOS mRNA expression was not affected. In addition, plasmid‑mediated overexpression of miR‑101 and small hairpin RNA‑mediated inhibition of c‑FOS significantly inhibited the proliferation and invasive capacity of T24 cells, as indicated by an MTT and a Transwell assay, respectively. However, plasmid‑mediated overexpression of c‑FOS reversed the inhibitory effects of miR‑101 overexpression on T24‑cell proliferation and invasion. In conclusion, the present study demonstrated that miR‑101 inhibits the proliferation and invasion of bladder cancer cells, at least partly via targeting c‑FOS, suggesting that miR-101/c‑FOS signaling may represent a potential therapeutic target for bladder cancer.