Unknown

Dataset Information

0

Epigallocatechin-3-Gallate Therapeutic Potential in Cancer: Mechanism of Action and Clinical Implications.


ABSTRACT: Cellular signaling pathways involved in the maintenance of the equilibrium between cell proliferation and apoptosis have emerged as rational targets that can be exploited in the prevention and treatment of cancer. Epigallocatechin-3-gallate (EGCG) is the most abundant phenolic compound found in green tea. It has been shown to regulate multiple crucial cellular signaling pathways, including those mediated by EGFR, JAK-STAT, MAPKs, NF-κB, PI3K-AKT-mTOR, and others. Deregulation of the abovementioned pathways is involved in the pathophysiology of cancer. It has been demonstrated that EGCG may exert anti-proliferative, anti-inflammatory, and apoptosis-inducing effects or induce epigenetic changes. Furthermore, preclinical and clinical studies suggest that EGCG may be used in the treatment of numerous disorders, including cancer. This review aims to summarize the existing knowledge regarding the biological properties of EGCG, especially in the context of cancer treatment and prophylaxis.

SUBMITTER: Kciuk M 

PROVIDER: S-EPMC10343677 | biostudies-literature | 2023 Jul

REPOSITORIES: biostudies-literature

altmetric image

Publications

Epigallocatechin-3-Gallate Therapeutic Potential in Cancer: Mechanism of Action and Clinical Implications.

Kciuk Mateusz M   Alam Manzar M   Ali Nemat N   Rashid Summya S   Głowacka Pola P   Sundaraj Rajamanikandan R   Celik Ismail I   Yahya Esam Bashir EB   Dubey Amit A   Zerroug Enfale E   Kontek Renata R  

Molecules (Basel, Switzerland) 20230706 13


Cellular signaling pathways involved in the maintenance of the equilibrium between cell proliferation and apoptosis have emerged as rational targets that can be exploited in the prevention and treatment of cancer. Epigallocatechin-3-gallate (EGCG) is the most abundant phenolic compound found in green tea. It has been shown to regulate multiple crucial cellular signaling pathways, including those mediated by EGFR, JAK-STAT, MAPKs, NF-κB, PI3K-AKT-mTOR, and others. Deregulation of the abovemention  ...[more]

Similar Datasets

| S-EPMC5534279 | biostudies-literature
| S-EPMC9785876 | biostudies-literature
| S-EPMC4897892 | biostudies-other
| S-EPMC9470551 | biostudies-literature
| S-EPMC5556358 | biostudies-other
2024-07-17 | GSE208144 | GEO
| S-EPMC5504484 | biostudies-literature
| S-EPMC1895573 | biostudies-literature
| S-EPMC9181147 | biostudies-literature
| S-EPMC10778335 | biostudies-literature