Honglin Xiang's scientific contributionswhile working at Hunan University (Changsha, China) and other institutions

Publications (2)

Publications citing this author (31)

    • In another study, it was found that genistein exerts significant antitumor effects in H446 small-cell lung cancer cells partially through inhibition of the FoxM1 pathway [147] . A novel synthetic genistein derivative, 7-difluoromethoxyl- 5,4 -di-n-octylgenistein, inactivated the FoxM1 signaling pathway in human ovarian cancer cells [148]. 3,3-Diindolylmethane (DIM) has also been reported to downregulate FoxM1 in DIM-treated breast cancer cells [149].
    [Show abstract] [Hide abstract] ABSTRACT: The association between chronic inflammation and cancer development has been well documented. One of the major obstacles in cancer treatment is the persistent autocrine and paracrine activation of pro-inflammatory transcription factors such as nuclear factor-κB, signal transducer and activator of transcription 3, activator protein 1, fork head box protein M1, and hypoxia-inducible factor 1α in a wide variety of tumor cell lines and patient specimens. This, in turn, leads to an accelerated production of cellular adhesion molecules, inflammatory cytokines, chemokines, anti-apoptotic molecules, and inducible nitric oxide synthase. Numerous medicinal plant-derived compounds have made a tremendous impact in drug discovery research endeavors, and have been reported to modulate the activation of diverse oncogenic transcription factors in various tumor models. Moreover, novel therapeutic combinations of standard chemotherapeutic drugs with these agents have significantly improved patient survival by making cancer cells more susceptible to chemotherapy and radiotherapy. In this review, we critically analyze the existing literature on the modulation of diverse transcription factors by various natural compounds and provide views on new directions for accelerating the discovery of novel drug candidates derived from Mother Nature.
    Full-text · Article · Mar 2016
    • by casticin may inhibit microtubule dynamics. On this basis, casticin has been shown to inhibit the proliferation of breast cancer, lung cancer, colon cancer, human myelogenous leukemia cells and hepatocellular carcinoma cells in vitro[20][21][22][23][24][31][32][33]. These findings suggest a similar anti-apoptotic inhibitory effect of casticin on rapid-proliferating cell types.
    [Show abstract] [Hide abstract] ABSTRACT: Although many advances have been made in understanding the pathogenesis of liver fibrosis, few options are available for treatment. Casticin, one of the major flavonoids in Fructus Viticis extracts, has shown hepatoprotective potential, but its effects on liver fibrosis are not clear. In this study, we investigated the antifibrotic activity of casticin and its underlying mechanism in vivo and in vitro. Male mice were injected intraperitoneally with carbon tetrachloride (CCl4) or underwent bile duct ligation (BDL) to induce liver fibrosis, followed by treatment with casticin or vehicle. In addition, transforming growth factor-β1(TGF-β1)-activated LX-2 cells were used. In vivo experiments showed that treatment with casticin alone had no toxic effect while significantly attenuating CCl4-or BDL-induced liver fibrosis, as indicated by reductions in the density of fibrosis, hydroxyproline content, expression of α-SMA and collagen α1(I) mRNA. Moreover, casticin inhibited LX2 proliferation, induced apoptosis in a time- and dose-dependent manner in vitro. The underlying molecular mechanisms for the effect of casticin involved inhibition of hepatic stellate cell (HSC) activation and reduced the expression of matrix metalloproteinase (MMP)-2, MMP-9, tissue inhibitor of metalloproteinases (TIMP)-1 and TIMP-2 resulting from blocking TGF-β1/Smad signaling, as well as increased the apoptosis of HSCs. The results suggest that casticin has potential benefits in the attenuation and treatment of liver fibrosis.
    Full-text · Article · Apr 2017