Role of Epigallocatechin Gallate in Glucose, Lipid, and Protein Metabolism and L-Theanine in the Metabolism-Regulatory Effects of Epigallocatechin Gallate

Li, Gang; Zeng, Li; Liu, An; Yuan, Dongyin; Peng, Yingqi; Zhang, Sheng; Li, Yinhua; Chen, Jinhua; Xiao, Wenjun; Gong, Zhihua

doi:10.3390/nu13114120

Cited by 7 publications

(4 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous studies showed that EGCG could target glucose metabolism in various types of cancers by reducing the activity and levels of vital glycolytic enzymes including hexokinase (HK), phosphofructokinase (PFK), lactic dehydrogenase (LDH), and pyruvate kinase (Lin et al, 2021; Wei et al, 2018; Wei et al, 2019). More recent studies reported that cellular energy metabolism changes, particularly abnormal glycolysis, and mitochondrial oxidative phosphorylation, were linked to cancer drug resistance (Martinez‐Outschoorn et al, 2017; Peng et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

Epigallocatechin gallate circumvents drug‐induced resistance in non‐small‐cell lung cancer by modulating glucose metabolism and AMPK/AKT/MAPK axis

Zhou,

Huang,

Guo

et al. 2023

Phytotherapy Research

View full text Add to dashboard Cite

Upon prolonged use of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) in non‐small‐cell lung cancer (NSCLC), acquired drug resistance inevitably occurs. This study investigates the combined use of EGFR‐TKIs (gefitinib or osimertinib) with epigallocatechin gallate (EGCG) to overcome acquired drug resistance in NSCLC models. The in vitro antiproliferative effects of EGFR‐TKIs and EGCG combination in EGFR‐mutant parental and resistant cell lines were evaluated. The in vivo efficacy of the combination was assessed in xenograft mouse models derived from EGFR‐TKI‐resistant NSCLC cells. We found that the combined use of EGFR‐TKIs and EGCG significantly reversed the Warburg effect by suppressing glycolysis while boosting mitochondrial respiration, which was accompanied by increased cellular ROS and decreased lactate secretion. The combination effectively activated the AMPK pathway while inhibited both ERK/MAPK and AKT/mTOR pathways, leading to cell cycle arrest and apoptosis, particularly in drug‐resistant NSCLC cells. The in vivo results obtained from mouse tumor xenograft model confirmed that EGCG effectively overcame osimertinib resistance. This study revealed that EGCG suppressed cancer bypass survival signaling and altered cancer metabolic profiles, which is a promising anticancer adjuvant of EGFR‐TKIs to overcome acquired drug resistance in NSCLC.

show abstract

Section: Discussionmentioning

confidence: 99%

Epigallocatechin gallate circumvents drug‐induced resistance in non‐small‐cell lung cancer by modulating glucose metabolism and AMPK/AKT/MAPK axis

Zhou,

Huang,

Guo

et al. 2023

Phytotherapy Research

View full text Add to dashboard Cite

show abstract

“…In the case of glycolysis, EGCG activates AMPK through regulating LKB1, and the activation of AMPK subsequently phosphorylates PFK. The inhibition of fatty acid and cholesterol synthesis induced by EGCG is achieved by ACC1 and HMG-CoA reductase (HMGCR) through the LKB1/AMPK signaling pathway [ 225 ]. EGCG was also found to inhibit autophagic processes in human melanoma skin A375 cells by inhibiting AMPK phosphorylation [ 226 ].…”

Section: Potential Ampk Modulators Of Natural Products From Herbal Me...mentioning

confidence: 99%

Novel Anti-Cancer Products Targeting AMPK: Natural Herbal Medicine against Breast Cancer

et al. 2023

View full text Add to dashboard Cite

Breast cancer is a common cancer in women worldwide. The existing clinical treatment strategies have been able to limit the progression of breast cancer and cancer metastasis, but abnormal metabolism, immunosuppression, and multidrug resistance involving multiple regulators remain the major challenges for the treatment of breast cancer. Adenosine 5′-monophosphate (AMP)-Activated Protein Kinase (AMPK) can regulate metabolic reprogramming and reverse the “Warburg effect” via multiple metabolic signaling pathways in breast cancer. Previous studies suggest that the activation of AMPK suppresses the growth and metastasis of breast cancer cells, as well as stimulating the responses of immune cells. However, some other reports claim that the development and poor prognosis of breast cancer are related to the overexpression and aberrant activation of AMPK. Thus, the role of AMPK in the progression of breast cancer is still controversial. In this review, we summarize the current understanding of AMPK, particularly the comprehensive bidirectional functions of AMPK in cancer progression; discuss the pharmacological activators of AMPK and some specific molecules, including the natural products (including berberine, curcumin, (−)-epigallocatechin-3-gallate, ginsenosides, and paclitaxel) that influence the efficacy of these activators in cancer therapy; and elaborate the role of AMPK as a potential therapeutic target for the treatment of breast cancer.

show abstract

“…Epigallocatechin gallate (EG) is considered as the most abundant polyphenol with bioactivity in green tea isolated from Camellia sinensis [ 15 ]. As a bioactive dietary component, EG owns a great many pharmacological actions including antioxidation, anti-inflammation, antifibrosis, and inhibiting endoplasmic reticulum stress [ 16 – 18 ].…”

Section: Introductionmentioning

confidence: 99%

Epigallocatechin Gallate Relieved PM2.5-Induced Lung Fibrosis by Inhibiting Oxidative Damage and Epithelial-Mesenchymal Transition through AKT/mTOR Pathway

Zhongyin

Wang

Juan

et al. 2022

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

Oxidative damage and epithelial-mesenchymal transition (EMT) are main pathological processes leading to the development of PM2.5-induced lung fibrosis. Epigallocatechin gallate (EG), a natural polyphenol extracted from green tea, possesses the ability to combat oxidative stress and inflammation. However, the potential roles of EG in PM2.5-induced lung fibrosis have not been reported yet. In the present study, we investigated whether EG could relieve PM2.5-induced lung injury and fibrosis in vivo and in vitro. To mimic PM2.5-induced lung fibrosis, C57/BL6 mice were intranasally instilled with PM2.5 suspension, and MLE-12 lung epithelial cells were stimulated with PM2.5 (100 μg/mL) in vitro. The results showed that intragastric administration of EG (20 mg/kg/d or 80 mg/kg/d for 8 weeks) significantly prevented lung injury, inflammation, and oxidative stress in PM2.5-induced mice, apart from inhibiting collagen deposition. Additionally, EG treatment also suppressed the activation of AKT/mTOR signaling pathway in lung tissues challenged with PM2.5. In vitro experiments further demonstrated that EG treatment could enhance cell viability in a concentration-dependent manner in PM2.5-treated MLE-12 lung epithelial cells. Also, the overexpression of constitutively active AKT could offset the inhibitory effects of EG on EMT and oxidative stress in PM2.5-treated MLE-12 lung epithelial cells. Finally, AKT overexpression also blocked the inhibitory effect of EG on the phosphorylation of mTOR in PM2.5-treated MLE-12 lung epithelial cells. In conclusion, EG could improve PM2.5-induced lung fibrosis by decreasing oxidative damage and EMT through AKT/mTOR pathway, which might be a potential candidate for the treatment of PM2.5-induced lung fibrosis.

show abstract

Role of Epigallocatechin Gallate in Glucose, Lipid, and Protein Metabolism and L-Theanine in the Metabolism-Regulatory Effects of Epigallocatechin Gallate

Cited by 7 publications

References 50 publications

Epigallocatechin gallate circumvents drug‐induced resistance in non‐small‐cell lung cancer by modulating glucose metabolism and AMPK/AKT/MAPK axis

Epigallocatechin gallate circumvents drug‐induced resistance in non‐small‐cell lung cancer by modulating glucose metabolism and AMPK/AKT/MAPK axis

Novel Anti-Cancer Products Targeting AMPK: Natural Herbal Medicine against Breast Cancer

Epigallocatechin Gallate Relieved PM2.5-Induced Lung Fibrosis by Inhibiting Oxidative Damage and Epithelial-Mesenchymal Transition through AKT/mTOR Pathway

Contact Info

Product

Resources

About