(−)-Epigallocatechin-3-gallate inhibits invasion and migration of salivary gland adenocarcinoma cells

Park, Jong‐Hwan; Yoon, Ji-Hye; Kim, Soo‐A; Ahn, Sang‐Gun; Yoon, Jung‐Hoon

doi:10.3892/or_00000673

Cited by 10 publications

(1 citation statement)

References 36 publications

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“…EGCG can also affect the expression and activity of MMPs by regulating numerous signaling pathways, including AKT, ERK, and NF-κB [8]. Park et al found that EGCG could inhibit the abnormally active FAK, AKT and ERK signaling pathways by down-regulating the dose-dependent expression level of integrin β 1, thereby decreasing the expression levels of MMP-2 and MMP-9 [9].NF-κB is an oxidative stress transcription factor involved in the regulation of a variety of important physiological processes, including apoptosis, inflammation, and autoimmunity, and in the study of oral cancer, the NF-κB signaling pathway was mainly involved in the inhibitory effect of EGCG on the overexpression of MMP-2 and MMP-9 [8].…”

Section: Regulation Of Matrix Metalloproteinasesmentioning

confidence: 99%

Progress in the Study of the Cariogenic Effect of Epigallocatechin Gallate

Wu,

Zhang,

Peng

et al. 2024

IJBLS

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Epigallocatechin gallate (EGCG), a compound rich in tea, has long been recognized for its diverse biological activities, including its remarkable antioxidant, anti-inflammatory, antibacterial, and anti-tumor properties. However, recent research has uncovered a new, promising application of EGCG: its role in the prevention of dental caries. This paper aims to comprehensively review the mechanisms underlying EGCG's involvement in caries development and progression, focusing on three key areas: its regulation of matrix metalloproteinases (MMPs), its inhibitory effects on Streptococcus mutans, and its promotion of dentin and enamel remineralization. Matrix metalloproteinases (MMPs) are a family of enzymes that play a crucial role in the degradation of extracellular matrix components. In the context of caries, MMPs are involved in the breakdown of tooth structure, facilitating the progression of the disease. EGCG has been shown to regulate MMP activity, thus potentially slowing down the destructive process associated with caries. By inhibiting MMPs, EGCG could help maintain the integrity of tooth structure and prevent further damage. Another significant aspect of EGCG's caries-preventive action is its inhibitory effect on Streptococcus mutans, a bacterium that plays a key role in caries development. S. mutans produces acids that erode tooth enamel, leading to caries formation. EGCG has been found to inhibit the growth of S. mutans and reduce its acid production, thereby reducing the risk of caries development. Lastly, EGCG promotes the remineralization of dentin and enamel. Remineralization is the process of depositing calcium and phosphate ions back into tooth structure, helping to repair damage caused by caries. EGCG has been shown to enhance this process, potentially leading to the reversal of early caries lesions and the restoration of tooth health.

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Section: Regulation Of Matrix Metalloproteinasesmentioning

confidence: 99%

Progress in the Study of the Cariogenic Effect of Epigallocatechin Gallate

Wu,

Zhang,

Peng

et al. 2024

IJBLS

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Developing and applying the adverse outcome pathway concept for understanding and predicting neurotoxicity

et al. 2017

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The Adverse Outcome Pathway (AOP) concept has recently been proposed to support a paradigm shift in regulatory toxicology testing and risk assessment. This concept is similar to the Mode of Action (MOA), in that it describes a sequence of measurable key events triggered by a molecular initiating event in which a stressor interacts with a biological target. The resulting cascade of key events includes molecular, cellular, structural and functional changes in biological systems, resulting in a measurable adverse outcome. Thereby, an AOP ideally provides information relevant to chemical structure-activity relationships as a basis for predicting effects of structurally similar compounds. AOPs could potentially also form the basis for qualitative and quantitative predictive modeling of the human adverse outcome resulting from molecular initiating or other key events for which higher-throughput testing methods are available or can be developed. A variety of cellular and molecular processes are known to be critical for normal function of the central (CNS) and peripheral nervous systems (PNS). Because of the biological and functional complexity of the CNS and PNS, it has been challenging to establish causative links and quantitative relationships between key events that comprise the pathways leading from chemical exposure to an adverse outcome in the nervous system. Following introduction of the principles of MOA and AOPs, examples of potential or putative adverse outcome pathways specific for developmental or adult neurotoxicity are summarized and aspects of their assessment considered. Their possible application in developing mechanistically informed Integrated Approaches to Testing and Assessment (IATA) is also discussed.

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Broad targeting of angiogenesis for cancer prevention and therapy

Wang

Dabrosin

Yin

et al. 2015

Seminars in Cancer Biology

415

332

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Deregulation of angiogenesis – the growth of new blood vessels from an existing vasculature – is a main driving force in many severe human diseases including cancer. As such, tumor angiogenesis is important for delivering oxygen and nutrients to growing tumors, and therefore considered an essential pathologic feature of cancer, while also playing a key role in enabling other aspects of tumor pathology such as metabolic deregulation and tumor dissemination/metastasis. Recently, inhibition of tumor angiogenesis has become a clinical anti-cancer strategy in line with chemotherapy, radiotherapy and surgery, which underscore the critical importance of the angiogenic switch during early tumor development. Unfortunately the clinically approved anti-angiogenic drugs in use today are only effective in a subset of the patients, and many who initially respond develop resistance over time. Also, some of the anti-angiogenic drugs are toxic and it would be of great importance to identify alternative compounds, which could overcome these drawbacks and limitations of the currently available therapy. Finding “the most important target” may, however, prove a very challenging approach as the tumor environment is highly diverse, consisting of many different cell types, all of which may contribute to tumor angiogenesis. Furthermore, the tumor cells themselves are genetically unstable, leading to a progressive increase in the number of different angiogenic factors produced as the cancer progresses to advanced stages. As an alternative approach to targeted therapy, options to broadly interfere with angiogenic signals by a mixture of non-toxic natural compound with pleiotropic actions were viewed by this team as an opportunity to develop a complementary anti-angiogenesis treatment option. As a part of the “Halifax Project” within the “Getting to know cancer” framework, we have here, based on a thorough review of the literature, identified 10 important aspects of tumor angiogenesis and the pathological tumor vasculature which would be well suited as targets for anti-angiogenic therapy: (1) endothelial cell migration/tip cell formation, (2) structural abnormalities of tumor vessels, (3) hypoxia, (4) lymphangiogenesis, (5) elevated interstitial fluid pressure, (6) poor perfusion, (7) disrupted circadian rhythms, (8) tumor promoting inflammation, (9) tumor promoting fibroblasts and (10) tumor cell metabolism/acidosis. Following this analysis, we scrutinized the available literature on broadly acting anti-angiogenic natural products, with a focus on finding qualitative information on phytochemicals which could inhibit these targets and came up with 10 prototypical phytochemical compounds: (1) oleanolic acid, (2) tripterine, (3) silibinin, (4) curcumin, (5) epigallocatechin-gallate, (6) kaempferol, (7) melatonin, (8) enterolactone, (9) withaferin A and (10) resveratrol. We suggest that these plant-derived compounds could be combined to constitute a broader acting and more effective inhibitory cocktail at doses that would not be likely to caus...

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(−)-Epigallocatechin-3-gallate inhibits invasion and migration of salivary gland adenocarcinoma cells

Cited by 10 publications

References 36 publications

Progress in the Study of the Cariogenic Effect of Epigallocatechin Gallate

Progress in the Study of the Cariogenic Effect of Epigallocatechin Gallate

Developing and applying the adverse outcome pathway concept for understanding and predicting neurotoxicity

Broad targeting of angiogenesis for cancer prevention and therapy

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