67-kDa Laminin Receptor Mediates the Beneficial Effects of Green Tea Polyphenol EGCG
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FOOD FACTORS: MOLECULAR TARGETS, MECHANISMS, PHARMACOLOGY AND IN VIVO EFFICACY (D-X HOU, SECTION EDITOR)
67-kDa Laminin Receptor Mediates the Beneficial Effects of Green Tea Polyphenol EGCG Motofumi Kumazoe 1 & Yoshinori Fujimura 1 & Hirofumi Tachibana 1
# Springer Nature Switzerland AG 2020
Abstract Purpose of Review Green tea is one of the most consumed beverages in the world. Through in vivo models and clinical trials, several studies have shown the beneficial effects of green tea. Epidemiological studies have revealed that green tea consumption is negatively correlated with the risk of cardiovascular diseases, stroke and cancer; however, little is known about the underlying molecular mechanisms. Recent Findings (−)-Epigallocatechin-3-O-gallate (EGCG) is one of the major bioactive compounds in green tea, and several studies emphasise its central role in the beneficial effects of green tea. It has been demonstrated that the 67-kDa laminin receptor, a non-integrin laminin receptor, mediates the beneficial effects of EGCG through cyclic guanosine monophosphate–dependent mechanisms. Summary In this review, we showed the role of 67LR as the sensor of the EGCG and its downstream cascade, and this review provides the recent findings in the mechanism of the beneficial effect of EGCG. Keywords EGCG . 67LR . cGMP . Cancer . Green tea . Polyphenol
Introduction EGCG is one of the major catechins in green tea and a characteristic polyphenol of this beverage [1]. Recently, several reports indicated that EGCG plays a central role in the beneficial effects of green tea including antioxidant [2], anticancer [3], anti-obesity [4], anti-allergy [5] and anti-inflammatory effects [6]. EGCG has a strong antioxidant effect, chemically reducing reactive oxygen species (ROS) [7]. This ROS regulation mechanism is thought to be one of the explanations for the cancer prevention effects of EGCG [8]. Chen et al. demonstrated that EGCG suppresses the cancer cells growth and
This article is part of the Topical Collection on Food Factors: Molecular Targets, mechanisms, pharmacology and in vivo efficacy * Hirofumi Tachibana [email protected] 1
Division of Applied Biological Chemistry, Department of Bioscience and Biotechnology, Faculty of Agriculture, Kyushu University, 744 Motooka, Nishi-ku, Fukuoka 819-0395, Japan
induces cell death without affecting normal cells [9], (Fig. 1). In the innate immune system, Toll-like receptor 4 (TLR4) recognises lipopolysaccharide, which is a common structure of Gram-negative bacteria and is also known as one of the endotoxins [10]. When triggered, TLR4 activates downstream signalling systems that finally trigger NFκb, the master regulator of inflammation-related genes [11]. Similar to what happens with TLR4, we hypothesised, in a previous study, the existence of a surficial receptor for the exogenous molecule EGCG. Because EGCG binds to cancer cells surface and this binding is strongly upregulated by all-trans-retinoic acid (ATRA), subtraction assays were performed with a base line sample and
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