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Wu H.-Y.,Nanjing University of Traditional Chinese Medicine | Wu H.-Y.,Yancheng Health Vocational and Technical College | Fan F.-T.,Nanjing University of Traditional Chinese Medicine | Liu Z.-G.,Nanjing University of Traditional Chinese Medicine | And 11 more authors.
Tumor | Year: 2014

The transcription factor forkhead box Q1 (FOXQ1), a member of foxhead box superfamily, widely exists in human tissues and organs, and it is involved in development process of embryonic stem cells and vertebrate. As a transcription factor, FOXQ1 protein activates the transcription by acting on promoter of target genes or interacting with other transcription factors, and it affects initiation, progression, invasion and metastasis of tumor cells in many aspects such as epithelial-mesenchymal transition (EMT) and cellular signal transduction. According to the relationship between FOXQ1 and tumors, the expression level of FOXQ1 can be used as a prognostic index for patients with certain tumors, and FOXQ1 is expected to be a novel target for tumor therapy. This review focuses on the role of FOXQ1 in initiation and progression of certain tumors as well as its potential mechanism, aiming to provide the valuable reference for anticancer treatment and research. Copyright© 2014 by TUMOR. Source


Liu Z.,Nanjing University | Zhu P.,Nanjing University | Zhu P.,Yangzhou University | Tao Y.,Nanjing University | And 15 more authors.
Food and Chemical Toxicology | Year: 2015

Epidemiologic and animal studies revealed that capsaicin (8-methyl-N-vanillyl-6-noneamide) can act as a carcinogen or cocarcinogen. However, the influence of consumption of capsaicin-containing foods or vegetables on skin cancer patients remains largely unknown. In the present study, we demonstrated that capsaicin has a cocarcinogenic effect on 9, 10-dimethylbenz[a]anthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate (TPA)-induced skin tumorigenesis. Our results showed that topical application of capsaicin on the dorsal skin of DMBA-initiated and TPA-promoted mice could significantly accelerate tumor formation and growth and induce more and larger skin tumors than the model group (DMBA + TPA). Moreover, capsaicin could promote TPA-induced skin hyperplasia and tumor proliferation. Mechanistic study found that inflammation-related factors cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) were highly elevated by pretreatment with capsaicin, suggesting an inflammation-dependent mechanism. Furthermore, mice that were administered capsaicin exhibited significant up-regulation of phosphorylation of nuclear factor kappaB (NF-κB), Erk and p38 but had no effect on JNK. Thus, our results indicated that inflammation, Erk and P38 collectively played a crucial role in cancer-promoting effect of capsaicin on carcinogen-induced skin cancer in mice. © 2015 Elsevier Ltd. Source


Ruan J.-S.,Nanjing University | Ruan J.-S.,Fujian Medical University | Liu Y.-P.,Nanjing University | Zhang L.,Nanjing University | And 8 more authors.
Acta Pharmacologica Sinica | Year: 2012

Aim:To investigate whether luteolin, a highly prevalent flavonoid, reverses the effects of epithelial-mesenchymal transition (EMT) in vitro and in vivo and to determine the mechanisms underlying this reversal.Methods:Murine malignant melanoma B16F10 cells were exposed to 1% O 2 for 24 h. Cellular mobility and adhesion were assessed using Boyden chamber transwell assay and cell adhesion assay, respectively. EMT-related proteins, such as E-cadherin and N-cadherin, were examined using Western blotting. Female C57BL/6 mice (6 to 8 weeks old) were injected with B16F10 cells (1×10 6 cells in 0.2 mL per mouse) via the lateral tail vein. The mice were treated with luteolin (10 or 20 mg/kg, ip) daily for 23 d. On the 23rd day after tumor injection, the mice were sacrificed, and the lungs were collected, and metastatic foci in the lung surfaces were photographed. Tissue sections were analyzed with immunohistochemistry and HE staining.Results:Hypoxia changed the morphology of B16F10 cells in vitro from the cobblestone-like to mesenchymal-like strips, which was accompanied by increased cellular adhesion and invasion. Luteolin (550 μmol/L) suppressed the hypoxia-induced changes in the cells in a dose-dependent manner. Hypoxia significantly decreased the expression of E-cadherin while increased the expression of N-cadherin in the cells (indicating the occurrence of EMT-like transformation), which was reversed by luteolin (5 μmol/L). In B16F10 cells, luteolin up-regulated E-cadherin at least partly via inhibiting the β3 integrin/FAK signal pathway. In experimental metastasis model mice, treatment with luteolin (10 or 20 mg/kg) reduced metastatic colonization in the lungs by 50%. Furthermore, the treatment increased the expression of E-cadherin while reduced the expression of vimentin and β3 integrin in the tumor tissues.Conclusion:Luteolin inhibits the hypoxia-induced EMT in malignant melanoma cells both in vitro and in vivo via the regulation of β3 integrin, suggesting that luteolin may be applied as a potential anticancer chemopreventative and chemotherapeutic agent. © 2012 CPS and SIMM. Source


Li W.D.,Nanjing University | Wu Y.,Nanjing University | Zhang L.,Anhui Provincial Hospital | Yan L.G.,Nanjing University | And 11 more authors.
Phytomedicine | Year: 2013

Anti-cancer investigations on Xanthatin mainly focus on in vitro experiments. We herein reported the anti-tumor effects of Xanthatin both in vitro and in vivo. MTS assay results showed that Xanthatin had a remarkable anti-proliferative effect on B16-F10 cells. Moreover, the expression of β-catenin was up-regulated both in vitro and in vivo. Animal studies further revealed that Xanthatin killed the tumor cells around the blood vessels which contributes to reduce microvascular density extremely. All these results indicate that Xanthatin inhibited murine melanoma B16-F10 cell proliferation possibly associated with activation of Wnt/β-catenin pathway and its activity against melanoma tumor might also be relevant to inhibition of angiogenesis. © 2013 Elsevier GmbH. All rights reserved. Source


Liu Z.-G.,Nanjing University of Traditional Chinese Medicine | Tao Y.,Nanjing University of Traditional Chinese Medicine | Wu H.-Y.,Nanjing University of Traditional Chinese Medicine | Wei Z.-H.,Nanjing University of Traditional Chinese Medicine | And 7 more authors.
Tumor | Year: 2014

Pepper is commonly used as spices and seasoning in people's daily life, and its main pungent component is capsaicin. Recent studies have suggested that capsaicin has broad pharmacological effects, including pain and itch relief, anti-inflammation, anti-oxidation and regulation of blood pressure. In recent years, research results showed that, capsaicin can not only inhibit the growth of malignant tumors, but also inhibit tumor angiogenesis both in vivo and in vitro . This article mainly reviews the recent progress in capsaicin and its receptors as well as their associations with cancer. The clinical limitation of capsaicin and its potential harmfulness of eating capsaicin are also discussed in this article, which may provide valuable references for future studies for investigators being engaged in cancer research. Copyright © 2014 by TUMOR. Source

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