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Liu J.,Chinese Peoples Liberation Army | Li J.,Huazhong University of Science and Technology | Zeng X.,General Hospital of the Yangtze River Shipping | Rao Z.,Chinese Peoples Liberation Army | And 7 more authors.
Inflammation | Year: 2014

In order to understand how tumor cells can escape immune surveillance mechanisms and thus develop antitumor therapies, it is critically important to investigate the mechanisms by which the immune system interacts with the tumor microenvironment. In our current study, wild-type mice were inoculated with melanoma cell line B16-F10 (1×106/mouse) and treated with the formyl peptide receptor (FPR) agonist WKYMVm or the FPR antagonist WRW 4. Growth of melanoma cell line B16-F10 was significantly inhibited in WKYMVm-treated mice and markedly promoted in WRW4-treated mice compared with control. Decreased number of myeloid-derived suppressor cells (MDSCs) and increased NK cell infiltration in tumor tissues were detected from WKYMVm-treated mice. Next, we showed that depletion of NK cell significantly increased tumor development in B16 tumor-bearing mice compared with the control group, and the suppressed tumor-developing effect of WKYMVm in B16 melanoma was abrogated with NK cell depletion. We also found that WKYMVm stimulates chemotactic migration in NK cells via the FPR family, and this was dependent on extracellular signal-related kinase (ERK) activation. Moreover, in our further experiment, we showed that the increased infiltration of NK cell and promoted NK cell chemotaxis in B16 melanoma induced by WKYMVm were both abolished with ERK inhibitor PD98059 administration. In conclusion, the FPR family promoted NK cell migration through ERK activation and inhibited B16 melanoma growth in a murine model. © 2014 Springer Science+Business Media. Source


Huang X.-F.,General Hospital of the Yangtze River Shipping | Yuan S.-J.,General Hospital of the Yangtze River Shipping | Yang C.,Huazhong University of Science and Technology
Chinese Journal of Tissue Engineering Research | Year: 2013

Background: PI3K/Akt pathway may play an important regulative role in osteogenic differentiation of dental pulp stem cells induced by drynaria total flavonoid. Objective: To explore the effects of total flavonoids of drynaria on osteogenic differentiation of rat dental pulp stem cells and investigate the role of PI3K/Akt pathway in the induced differentiation of rat dental pulp stem cells. Methods: Rat dental pulp stem cells were harvested by enzymatic digestion, cultured and identified by immunohistochemical staining. The dental pulp stem cells were cultured in media with different concentrations of drynaria total flavonoid (0.01 g/L, 0.05 g/L and 0.1 g/L). Alkaline phosphatase activities and formation of calcified tubercles in cells were determined in each group. Phosphorylated Akt expression in cells was detected by western blot method in each group. Results and Conclusion: Dental pulp stem cells were positive for CD44 and CD29 expression, but they were negative for CD34. Compared to the blank control group, alkaline phosphatase activities, formation of calcified tubercles and phosphorylated Akt expression were significantly increased in the drynaria total flavonoid group in a dose- and time-dependent manner. These findings suggest that drynaria total flavonoid can promote the osteogenic differentiation of rat dental pulp stem cells, and this effect is likely mediated by PI3K/Akt pathway. Source


Huang X.-F.,General Hospital of the Yangtze River Shipping | Yuan S.-J.,General Hospital of the Yangtze River Shipping | Yang C.,Huazhong University of Science and Technology
Molecular Medicine Reports | Year: 2012

Dental pulp stem cells (DPSCs) have the potential to form bone, nerve and fat, and are a candidate for use in regenerative medicine. Previous studies indicated that total flavonoids from Drynaria fortunei show a stimulative effect on the proliferation and osteogenic differentiation of osteoblastic MC3T3-E1 cells in vitro. This study aimed to investigate the effect of total flavonoids from Drynaria fortunei on the proliferation and osteogenic differentiation of rat DPSCs, and to further clarify the mechanisms involved. DPSCs were isolated by enzymatic digestion and identified using the CD44, CD29 and CD34 markers by immunohistochemistry, and exposed to 0.01, 0.05 and 0.1 g/l total flavonoids from Drynaria fortunei media. Total flavonoids from Drynaria fortunei promoted the proliferation of DPSCs in a dose-dependent manner and this effect may depend on the shortening of the G0/G1 phase and promotion of the S phase. Compared with the control group, the levels of alkaline phosphatase (ALP) and the expression of osteogenic genes increased with the concentrations of total flavonoids from Drynaria fortunei, and the volume and number of calcified nodules in the Drynaria groups was bigger compared to the control group. These results suggest that total flavonoid from Drynaria fortunei directly stimulates DPSC proliferation and osteogenic differentiation, and may serve as a new promising candidate drug for dental tissue engineering and bone regeneration. Source


Peng J.-J.,General Hospital of the Yangtze River Shipping | Wu B.,The First Hospital of Wuhan City | Xiao X.-B.,The First Hospital of Wuhan City | Shao Y.-S.,The First Hospital of Wuhan City | And 2 more authors.
Archives of Medical Research | Year: 2014

Background and Aims: To investigate the expression and prognostic significance of Krüppel-like factor 17 (KLF17) in human gastric cancer. Methods: KLF17 expressions in 158 paraffin-embedded gastric cancer samples were analyzed using immunohistochemistry. In addition, KLF17 expressions patterns in three fresh gastric cancer tissues and noncancerous gastric mucosa were examined by Western blotting. The correlation between KLF17 expression and clinicopathological factors as well as patient survival was investigated. Results: Immunohistochemical staining data indicated that KLF17 expression was significantly decreased in 98 of 158 gastric adenocarcinoma cases. Reduced KLF17 expression in fresh gastric cancer tissues was confirmed by Western blotting. Reduced expression of KLF17 was strongly correlated with tumor size, pN stage and lymphovascular invasion. Multivariate Cox regression analysis identified KLF17 expression as an independent prognostic factor for both overall survival (HR = 0.481, 95% CI = 0.225-0.665, p = 0.009) and disease-free survival (HR = 0.438, 95% CI = 0.254-0.758, p = 0.003). Conclusion: The reduced expression of KLF17 protein in gastric cancer was correlated with tumor size, pN stage and lymphovascular invasion and was an independent predictor for poor survival in patients undergoing surgery for gastric cancer. © 2014 IMSS. Source


Pu F.,Huazhong University of Science and Technology | Chen F.,General Hospital of the Yangtze River Shipping | Chen S.,Huazhong University of Science and Technology | Wang B.,Huazhong University of Science and Technology | And 2 more authors.
OncoTargets and Therapy | Year: 2015

Objective: The aim of this study was to evaluate the relationship between GSTP1 polymorphisms and prognosis of osteosarcoma in patients treated with chemotherapy, by performing a meta-analysis. Methods: The studies of effects of GSTP1 gene polymorphisms on osteosarcoma survival after chemotherapy were collected. STATA (version 12.0) was used to perform data synthesis. Results: Six studies involving 898 participants were included. A meta-analysis was performed on studies in GSTP1 313A>G(rs1695) assessing the association between tumor response and the polymorphisms in GSTP1 (AA vs AG, AA vs GG), the pooled odds ratios (ORs) were 2.06 (95% confidence interval [CI]: 1.48–2.86, P=0.628, I2=0.0%). There was significant association between the polymorphisms in GSTP1 (AA vs AG, AA vs GG) and the events that happened, the pooled ORs were 1.86 (95% CI: 1.14–3.06, P=0.034, I2=58.6%), and there was significant association between the polymorphisms in GSTP1 (AA vs AG, AA vs GG) and survival times (overall survival and progression-free survival) in osteosarcoma patients treated with chemotherapy, and the pooled ORs were 2.14 (95% CI: 1.51–3.04, P=0.675, I2=0.0%) and 2.77 (95% CI: 1.56–4.91, P=0.347, I2=9.3%), respectively. Two studies assessed the association of polymorphisms in GSTP1 I105V (IIe/IIe vs IIe/Val, IIe/IIe vs Val/Val) with overall survival in human osteosarcoma. The pooled ORs were 1.20 (95% CI: 0.64–2.27, P=0.010, I2=73.5%). The study showed an insignificant difference in overall survival for the polymorphisms in GSTP1 (IIe/IIe vs IIe/Val, IIe/IIe vs Val/Val). Conclusion: This meta-analysis indicated that GSTP1 polymorphisms might influence osteosarcoma risk and suggests that GSTP1 polymorphisms may be an important risk factor for osteosarcoma. © 2015 Pu et al. Source

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