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The Genus Letrouitia (Letrouitiaceae: Lichenized Ascomycota) New to Cambodia
Shi, Haixia,Qian, Zigang,Wang, Xinyu,Liu, Dong,Zhang, Yanyun,Ye, Xin,Harada, Hiroshi,Wang, Lisong The Korean Society of Mycology 2015 Mycobiology Vol.43 No.2
The genus Letrouitia is newly recorded for Cambodia, including the four species as L. domingensis, L. leprolytoides, L. sayeri, and L. subvulpina. A brief description and illustrations are provided.
Signal Transduction Pathways: Targets for Green and Black Tea Polyphenols
Bode, Ann M.,Dong, Zigang Korean Society for Biochemistry and Molecular Biol 2003 Journal of biochemistry and molecular biology Vol.36 No.1
Tea is one of the most popular beverages consumed in the world and has been demonstrated to have anti-cancer activity in animal models. Research findings suggest that the polyphenolic compounds, (-)-epigallocatechin-3-gallate, found primarily in green tea, and theaflavin-3,3'-digallate, a major component of black tea, are the two most effective anti-cancer factors found in tea. Several mechanisms to explain the chemopreventive effects of tea have been presented but others and we suggest that tea components target specific cell-signaling pathways responsible for regulating cellular proliferation or apoptosis. These pathways include signal transduction pathways leading to activator protein-1 (AP-1) and/or nuclear factor kappa B(NF-${\kappa}B$ ). AP-1 and NF-${\kappa}B$ are transcription factors that are known to be extremely important in tumor promoter-induced cell transformation and tumor promotion, and both are influenced differentially by the MAP kinase pathways. The purpose of this brief review is to present recent research data from other and our laboratory focusing on the tea-induced cellular signal transduction events associated with the MAP kinase, AP-1, and NF-${\kappa}B$ pathways.
Signal Transduction Pathways : Targets for Green and Black Tea Polyphenols
Bode, Ann M.,Dong, Zigang 한국생화학분자생물학회 2003 BMB Reports Vol.36 No.1
Tea is one of the most popular beverages consumed in the world and has been demonstrated to have anti-cancer activity in animal models. Research findings suggest that the polyphenolic compounds, (-)-epigallocatechin-3-gallate found primarily in green tea, and theaflavin-3, 3'-digallate, a major component of black tea, are the two most effective anti-cancer factors found in tea. Several mechanisms to explain the chemopreventive effects of tea have been presented but others and we suggest that tea components target specific cell-signaling pathways responsible for regulating cellular proliferation or apoptosis. These pathways include signal transduction pathways leading to activator protein-1 (AP-1) and/or nuclear factor kappa B (NF-κB). AP-1 and NF-κB are transcription factors that are known to be extremely important in tumor promoter-induced cell transformation and tumor promotion, and both are influenced differentially by the MAP kinase pathways. The purpose of this brief review is to present recent research data from other and our laboratory focusing on the tea-induced cellular signal transduction events associated with the MAP kinase, AP-a, and NF-κB pathways.
Benefits of Soybean in the Era of Precision Medicine: A Review of Clinical Evidence
Kang Jung Hyun,Dong Zigang,Shin Seung Ho 한국미생물·생명공학회 2023 Journal of microbiology and biotechnology Vol.33 No.12
Soybean (Glycine max) is an important ingredient of cuisines worldwide. While there is a wealth of evidence that soybean could be a good source of macronutrients and phytochemicals with healthpromoting effects, concerns regarding adverse effects have been raised. In this work, we reviewed the current clinical evidence focusing on the benefits and risks of soybean ingredients. In breast, prostate, colorectal, ovarian, and lung cancer, epidemiological studies showed an inverse association between soybean food intake and cancer risks. Soybean intake was inversely correlated with risks of type 2 diabetes mellitus (T2DM), and soy isoflavones ameliorated osteoporosis and hot flashes. Notably, soybean was one of the dietary protein sources that may reduce the risk of breast cancer and T2DM. However, soybean had adverse effects on certain types of drug treatment and caused allergies. In sum, this work provides useful considerations for planning clinical soybean research and selecting dietary protein sources for human health.
Cocoa procyanidins suppress transformation by inhibiting mitogen-activated protein kinase kinase.
Kang, Nam Joo,Lee, Ki Won,Lee, Dong Eun,Rogozin, Evgeny A,Bode, Ann M,Lee, Hyong Joo,Dong, Zigang American Society for Biochemistry and Molecular Bi 2008 The Journal of biological chemistry Vol.283 No.30
<P>Cocoa was shown to inhibit chemically induced carcinogenesis in animals and exert antioxidant activity in humans. However, the molecular mechanisms of the chemopreventive potential of cocoa and its active ingredient(s) remain unknown. Here we report that cocoa procyanidins inhibit neoplastic cell transformation by suppressing the kinase activity of mitogen-activated protein kinase kinase (MEK). A cocoa procyanidin fraction (CPF) and procyanidin B2 at 5 mug/ml and 40 mum, respectively, inhibited 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced neoplastic transformation of JB6 P+ mouse epidermal (JB6 P+) cells by 47 and 93%, respectively. The TPA-induced promoter activity and expression of cyclooxygenase-2, which is involved in tumor promotion and inflammation, were dose-dependently inhibited by CPF or procyanidin B2. The activation of activator protein-1 and nuclear factor-kappaB induced by TPA was also attenuated by CPF or procyanidin B2. The TPA-induced phosphorylation of MEK, extracellular signal-regulated kinase, and p90 ribosomal s6 kinase was suppressed by CPF or procyanidin B2. In vitro and ex vivo kinase assay data demonstrated that CPF or procyanidin B2 inhibited the kinase activity of MEK1 and directly bound with MEK1. CPF or procyanidin B2 suppressed JB6 P+ cell transformation induced by epidermal growth factor or H-Ras, both of which are known to be involved in MEK/ERK signal activation. In contrast, theobromine (up to 80 mum) had no effect on TPA-induced transformation, cyclooxygenase-2 expression, the transactivation of activator protein-1 or nuclear factor-kappaB, or MEK. Notably, procyanidin B2 exerted stronger inhibitory effects compared with PD098059 (a well known pharmacological inhibitor of MEK) on MEK1 activity and neoplastic cell transformation.</P>
Ginsenosides and their metabolites: a review of their pharmacological activities in the skin.
Lim, Tae-Gyu,Lee, Charles C,Dong, Zigang,Lee, Ki Won Springer-Verlag 2015 Archives of dermatological research Vol.307 No.5
<P>Ginsenosides are representative pharmaceutical compounds found in various forms in Panax ginseng, a traditional medicinal plant. They are converted to their metabolites Rg2, Rg3, compound K, and others by human intestinal microflora following ingestion. Numerous studies have demonstrated beneficial effects of ginsenosides against aberrant molecular processes responsible for cancer, metabolic diseases and neurodegenerative diseases. Recently, antiaging effects of ginsenosides in human skin have been reported from clinical trial and in vitro model data. Ginsenosides have hence been proposed as promising natural cosmeceutical agents. In this review, we will critically review the known biological effects of several ginsenosides (Rb1, Rg3, Rd and compound K), such as anti-inflammatory and anticancer activities, which arise from the modulation of diverse molecular pathways. The application potential of ginsenosides as cosmeceutical ingredients will also be reviewed.</P>
Molecular targets of phytochemicals for cancer prevention
Lee, Ki Won,Bode, Ann M.,Dong, Zigang Nature Publishing Group, a division of Macmillan P 2011 Nature reviews. Cancer Vol.11 No.3
Although successful for a limited number of tumour types, the efficacy of cancer therapies, especially for late-stage disease, remains poor overall. Many have argued that this could be avoided by focusing on cancer prevention, which has now entered the arena of targeted therapies. During the process of identifying preventive agents, dietary phytochemicals, which are thought to be safe for human use, have emerged as modulators of key cellular signalling pathways. The task now is to understand how these chemicals perturb these pathways by modelling their interactions with their target proteins.
Lee, Mee-Hyun,Huang, Zunnan,Kim, Dong Joon,Kim, Sung-Hyun,Kim, Myoung Ok,Lee, Sung-Young,Xie, Hua,Park, Si Jun,Kim, Jae Young,Kundu, Joydeb Kumar,Bode, Ann M.,Surh, Young-Joon,Dong, Zigang American Association for Cancer Research 2013 Cancer prevention research Vol.6 No.5
<P>Abnormal functioning of multiple gene products underlies the neoplastic transformation of cells. Thus, chemopreventive and/or chemotherapeutic agents with multigene targets hold promise in the development of effective anticancer drugs. Silybin, a component of milk thistle, is a natural anticancer agent. In the present study, we investigated the effect of silybin on melanoma cell growth and elucidated its molecular targets. Our study revealed that silybin attenuated the growth of melanoma xenograft tumors in nude mice. Silybin inhibited the kinase activity of mitogen-activated protein kinase (MEK)-1/2 and ribosomal S6 kinase (RSK)-2 in melanoma cells. The direct binding of silybin with MEK1/2 and RSK2 was explored using a computational docking model. Treatment of melanoma cells with silybin attenuated the phosphorylation of extracellular signal-regulated kinase (ERK)-1/2 and RSK2, which are regulated by the upstream kinases MEK1/2. The blockade of MEK1/2-ERK1/2-RSK2 signaling by silybin resulted in a reduced activation of NF-κB, activator protein-1, and STAT3, which are transcriptional regulators of a variety of proliferative genes in melanomas. Silybin, by blocking the activation of these transcription factors, induced cell-cycle arrest at the G<SUB>1</SUB> phase and inhibited melanoma cell growth <I>in vitro</I> and <I>in vivo</I>. Taken together, silybin suppresses melanoma growth by directly targeting MEK- and RSK-mediated signaling pathways. <I>Cancer Prev Res; 6(5); 455–65. ©2013 AACR</I>.</P>