Abstract. Prostate cancer presents high occurrence worldwide. Medicinal plants are a major source of novel and potentially therapeutic molecules; therefore, the aim of the present study was to investigate the possible anti-prostate cancer activity of afzelin, a flavonol glycoside that was previously isolated from Nymphaea odorata. The effect of afzelin on the proliferation of androgen-sensitive LNCaP and androgen-independent PC-3 cells was evaluated by performing a water soluble tetrazolium salt-1 assay. In addition, the effect of afzelin on the cell cycle of the LNCaP and PC-3 prostate cancer cell lines was evaluated. Western blot analysis was performed to evaluate the effect of afzelin on the kinases responsible for the regulation of actin organization. Afzelin was identified to inhibit the proliferation of LNCaP and PC3 cells, and block the cell cycle in the G 0 phase. The anticancer activity of afzelin in these cells was determined to be due to inhibition of LIM domain kinase 1 expression. Thus, the in vitro efficacy of afzelin against prostate cancer is promising; however, additional studies on different animal models are required to substantiate its anticancer potential. IntroductionProstate cancer is the second most frequently diagnosed type of cancer and the sixth most common cause of cancer-associated mortality in males, worldwide (1). The typical treatment strategies of chemotherapy and radiotherapy have not provided significant survival benefits for patients with advanced prostate cancer, and the majority of available strategies are only palliative (2). Therefore, there is requirement for the prompt identification of novel molecules to treat the increasing number of prostate cancer cases, particularly cases that are resistant to current chemotherapeutic agents (3,4).Afzelin is a flavonol glycoside found in Nymphaea odorata, which has been identified to inhibit the growth of breast cancer cells by stimulating apoptosis (5). In addition, afzelin has been demonstrated to scavenge superoxide anion radicals in RAW264.7 cells (6). The structure of this compound is shown in Fig. 1.In eukaryotic cells, the actin cytoskeleton is essential for mediating various biological functions, including providing the structural framework of the cell, and driving cellular motility and division. In particular, dynamic reorganization of the actomyosin cytoskeleton and remodelling of the extracellular matrix drive the multistep process of tumor cell metastasis. Tumor cells are able to cross tissue boundaries into the blood and lymphatic systems and migrate to distal regions of the body. Therefore, cancer therapy has recently focused on gaining a comprehensive understanding of the biological processes that regulate actin organization (7).Rho GTPase family proteins are key regulators of the actin cytoskeleton and, with the aid of various target proteins, maintain the tight regulation of normal cell growth and differentiation (8-11). Eukaryotic cells exhibit a predisposition to rapid and uncontrollable growth following genomic a...
BackgroundThe results of studies on association between the polymorphisms in the coding region and the promoter of uridine diphosphateglucuronosyl transferase 1A1 (UGT1A1) and neonatal hyperbilirubinemia are controversial. This study aimed to determine whether the UGT1A1 gene polymorphisms of Gly71Arg and TATA promoter were significant risk factors associated with neonatal hyperbilirubinemia.Material/MethodsThe PubMed, Cochrane Library, and Embase databases were searched for papers that describe the association between UGT1A1 polymorphisms and neonatal hyperbilirubinemia. Summary odds ratios and 95% confidence intervals (CI) were estimated based on a fixed-effects model or random-effects model, depending on the absence or presence of significant heterogeneity.ResultsA total of 32 eligible studies and 6520 participants were identified. Among them, 24 studies focused on the association of neonatal hyperbilirubinemia with UGT1A1 Gly71Arg polymorphisms, and a significant difference was found for the comparison of AA vs. AG+GG (OR=3.47, 95% CI=2.29–5.28, P<0.0001). We included 19 studies on the association of neonatal hyperbilirubinemia with UGT1A1 TATA promoter polymorphism, which also found a statistically significant difference between 7/7 and 6/7 + 6/6 (OR=2.24, 95% CI=1.29–3.92, P=0.004).ConclusionsThis meta-analysis demonstrated that UGT1A1 polymorphisms (Gly71Arg and TATA promoter) significantly increase the risk of neonatal hyperbilirubinemia.
EGCG is one of the major catechins in green tea. In this study, we investigated the novel regulatory mechanism of EGCG on amelioration of experimental autoimmune encephalomyelitis (EAE). The data showed that EGCG reduced disease severity in EAE by decreasing brain inflammation and demyelination damage, accompanied by decreased encephalitogenic T cell responses and reduced expression of inflammatory cytokines and chemokines. The effect of EGCG was attributable to its selective inhibition of interferon-gamma and interleukin-17 production in CD4+ T cells, mediated via alteration of the STAT pathway and the transcription factors T-bet and retinoid-related orphan receptor (ROR) gammat/ROR alpha. More important, EGCG has been found novel properties of directly inhibiting Th1 and Th17 cell differentiation in this study. On the other hand, EGCG-treated antigen presenting cells (APC) exhibited reduced co-stimulatory function as a result of altered expression of CD80 and CD86. The results of this study indicate that EGCG is a novel anti-inflammatory agent that could act as a useful drug for the treatment of multiple sclerosis and other neuroinflammatory diseases in the further.
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