Potential Therapeutic Targets of Epigallocatechin Gallate (EGCG), the Most Abundant Catechin in Green Tea, and Its Role in the Therapy of Various Types of Cancer
Abstract
:1. Introduction
2. Main Mechanisms of EGCG in the Inhibition of Cancer
2.1. Inflammation
2.2. Reactive Oxygen Species (ROS)
2.3. Angiogenesis
2.4. Apoptosis
2.5. Tumor Suppressor Genes
2.6. Cell Cycle
Pathogenesis | Types of Genes | Mechanism | Refs. |
---|---|---|---|
Inflammation | Necrosis factor (TNF)-α/intercellular adhesion molecule-1 expression | EGCG protected against tumor necrosis factor-α-mediated lung inflammation through down-regulation of oxidative stress and intercellular adhesion molecule-1 expression | [5] |
Breast cancer | Vascular endothelial growth factor | EGCG have been proven to reduce vascular endothelial growth factor production | [14] |
Breast cancer | HIF-1α and NFκB | EGCG inhibited the activation of HIF-1α and NFκB and VEGF expression | [16] |
Laryngeal carcinoma cells/ Colon carcinoma cells/Cervical carcinoma cells | Apoptosis | EGCG was found to induce apoptosis in cells of the examined neoplastic cell lines in a dose-related manner | [20] |
Hepatocellular carcinoma | Bcl-2 and NF-κB | EGCG-induced apoptosis of cancer cells was linked with a substantial decrease in Bcl-2 and NF-κB expression | [21] |
Human prostate cancer | p53 | Epigallocatechin-3-gallate, activate p53 via acetylation at the Lys373 and Lys382 residues through inhibiting class I HDACs | [22] |
Lung cancer | p53 | EGCG play crucial role in the inhibition of anchorage-independent growth of human lung cancer cells through upregulating p53 expression | [23] |
Pancreatic cancer | Pten | EGCG is capable of decreasing proliferation and induce the apoptosis linked with the expression of PTEN. | [24] |
Pancreatic cancer | Pten | EGCG upregulate PTEN expression and downregulate the expression of pAKT and p-mTOR | [28] |
Pancreatic cancer | PI3K/Akt/mTOR pathway | EGCG subdue the expression of p-Akt and p-mTOR through PTEN to regulate the PI3K/Akt/mTOR pathway | [24] |
Biliary tract cancer | p21 | EGCG reduced the mRNA levels of various cell cycle-related genes, but enhanced the expression of the cell cycle inhibitor p21 | [26] |
2.7. Phosphatidylinositide-3-Kinases (PI3Ks)/AKT Pathways
2.8. Signal Transducer and Activator of Transcription 3 (STAT3)
2.9. Epidermal Growth Factor Receptor (EGFR)
2.10. Activating Protein-1 (AP-1)
2.11. Phase II Detoxifying Enzymes
3. Role of EGCG in Inhibition and Prevention of Various Types of Cancer
3.1. Cervix Cancer
3.2. Breast Cancer
3.3. Ovarian Cancer
3.4. Endometrium Cancer
3.5. Pancreatic Cancer
3.6. Gastric Cancer
3.7. Liver Cancer
3.8. Colon Cancer
3.9. Bile Duct Cancer
3.10. Renal Cancer
3.11. Prostate Cancer
3.12. Urinary Bladder Cancer
3.13. Leukemia
3.14. Lymphoma
3.15. Head and Neck Cancer
3.16. Oral Cancer
3.17. Oesophagus Cancer
3.18. Melanoma
3.19. Lung Cancer
3.20. Myeloma
3.21. Osteosarcoma
3.22. Brain Tumor
3.23. Endocrine Related Cancer
3.24. Retinoblastoma
4. In Vivo Efficacy of Epigallocatechin-Gallate (EGCG) in the Management of Cancer
5. Measurement of Safety, Efficacy and Tolerability of EGCG in Cancer Based on Human Clinical Trials
5.1. Prostate Cancer
5.2. Urinary Bladder Cancer
5.3. Head and Neck Cancer
5.4. Breast Cancer
5.5. Ovarian Cancer
5.6. Lung Cancer
6. Effect of EGCG Alone and in Combination with Other Anticancer Compounds or Related Molecules
7. Available Concentration and Improvement of Bioavailability of Epigallocatechin Gallate (EGCG)
7.1. Liposome/Nanoliposome
7.2. Nanoemulsion
7.3. Chitosan/Carbohydrate Based Carrier
7.4. Polymeric Nanoparticles
7.5. Serum Albumin and Caseins Used as a Carrier
7.6. Structural Modification of EGCG
8. Conclusions
Author Contributions
Funding
Acknowledgments
Conflicts of Interest
References
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Cancer Types | Study Type | Finding of the Study | Refs. |
---|---|---|---|
Cervix cancer | In vitro | EGCG with eugenol amrogentin greatly inhibit the cellular proliferation and colony formation | [44] |
Cervix cancer | In vitro | EGCG treatment causes down regulation of genes involved in the stimulation of proliferation and motility and invasion processes. | [46] |
Breast cancer | In vitro | EGCG reduced breast cancer cell growth in a concentration- and time dependent manner | [48] |
Breast cancer | In vitro | Epigallocatechin gallate powerfully inhibited the growth of cancer stem/progenitor cells. | [49] |
Breast cancer | In vitro | Protein expression of HIF-1α and VEGF dropped in cancer cells pre-treated with increasing concentrations of | [51] |
Ovarian cancer | In vitro | EGCG improved the toxicity of cisplatin and epigallocatechin-3-gallate increased cisplatin strength | [52] |
Ovarian cancer | In vitro | EGCG plays an important role in decreasing ovarian cancer cell growth. Correspondingly, Epigallocatechin gallate showed growth inhibitory effects in each cell line in a dose-dependent approach and induced apoptosis and cell cycle arrest | [56] |
Ovarian cancer | In vitro | Epigallocatechin-3-gallate causes a substantial task in decreasing cancer cell growth, showed dose dependent growth inhibitory effects | [57] |
Endometrial cancer | In vitro | EGCG caused the arrest of cells in the G0/G1 phase of the cell cycle | [62] |
Endometrial cancer | In vitro | EGCG was established to inhibit proliferation of adenocarcinoma cells | [63] |
Pancreatic cancer | In vitro | EGCG decreased pancreatic cancer cell migration, growth and invasion | [67] |
Pancreatic cancer | In vitro | EGCG reduced pancreatic cancer cell growth in a concentration-dependent manner | [68] |
Pancreatic cancer | In vitro | The synergistic activity was credited to the cell cycle arrest and the induction of the reactive oxygen species-dependent mitochondria mediated apoptosis | [70] |
Pancreatic cancer | In vitro | EGCG caused growth arrest at G1 stage of cell cycle, and induced apoptosis | [72] |
Gastric cancer | In vitro | EGCG was accomplished to inhibit vascular endothelial growth factor secretion and expression | [74] |
Gastric cancer | In vitro | EGCG significantly inhibited proliferation and increased apoptosis of cancer cells in vitro. | [75] |
Gastric cancer | In vitro | EGCG meaningfully promoted apoptosis and inhibited the proliferation | [77] |
Gastric cancer | In vitro | EGCG treatment reduced vascular endothelial growth factor protein level | [78] |
Gastric cancer | In vitro | Microvessel density in tumor tissues receiving epigallocatechin-3-gallate treatment was also evidently reduced and markedly reduced VEGF protein level | [79] |
Liver tumour | In vitro | The epigallocatechin gallate reduced hypoxia-incited apoptosis in HepG2 cells as well as enhanced cell survival | [82] |
Liver cancer | In vitro | Epigallocatechin gallate reduced expression of MMP-9, syndecan-1 and FGF-2 | [83] |
Colorectal cancer | In vitro | Epigallocatechin gallate and sodium butyrate combination treatment induced apoptosis and cell cycle arrest | [85] |
Colon cancer | In vitro | EGCG-induced downregulation of epidermal growth factor receptor cancer cells | [86] |
Colon cancer | In vitro | Both Epigallocatechin-3-gallate and Poly E initiated a decrease in the phosphorylated forms of EGFR | [87] |
Bile duct cancer | In vitro | JAK/STAT pathway activation through pro-inflammatory cytokine in cancer cells was decreased via pre-treatment with quercetin and epigallocatechin-3-gallate | [91] |
Bile duct cancer | In vitro | The combination of vorinostat and epigallocatechin-3-gallate revealed synergistic growth inhibitory effects and caused induction of apoptosis in tumor cells. | [92] |
Renal Cell Carcinoma | In vitro | Epigallocatechin-3-gallate inhibits growth and induces apoptosis | [94] |
Renal Cell Carcinoma | In vitro | EGCG showed potentiality to inhibit the proliferation, and induce apoptosis | [95] |
Renal Cell Carcinoma | In vitro | EGCG treatment provoked important upregulation of Cx32 in cancer cells | [97] |
Prostate Cancer | In vitro | EGCG induces apoptosis through triggering caspase and preventing the expression of Bcl-2 | [99] |
Prostate Cancer | In vitro | Epigallocatechin-3-gallate demonstrated low inhibitory effect on cancer cell proliferation | [100] |
Prostate Cancer | In vitro | EGCG showed anticancer effects and it was proved that epigallocatechin-3-gallate inhibited cancer cell proliferation | [102] |
Urinary bladder cancer | In vitro | Treatment of EGCG caused in important inhibition of cell proliferation via induction of apoptosis and inhibited cancer cell migration | [104] |
Urinary bladder cancer | In vitro | Epigallocatechin-3-gallate increased growth inhibition in a dose- and time-dependent manner | [105] |
Leukemia | In vitro | Proliferation and cell cycle progression of cancer cells treated with epigallocatechin-3-gallate were inhibited | [109] |
Leukemia | In vitro | Epigallocatechin-3-gallate treatment induced apoptosis and increased the levels of Bax protein expression | [111] |
Leukemia | In vitro | EGCG showed higher growth suppression and induced apoptosis demonstrated by nuclei fragmentation and nuclear fragmentation | [113] |
Lymphoma | In vitro | EGCG induced growth inhibition and apoptosis in a dose- and time-dependent way | [114] |
Lymphoma | In vitro | Epigallocatechin-3-gallate were able to inhibit the growth of malignancy cell lines | [115] |
Lymphoma | In vitro | EGCG caused induction of cell death and reactive oxygen species generation | [116] |
Head and neck cancer | In vitro | EGCG inhibits the self-renewal capacity and reduces the expression of stem cell markers | [118] |
Head and neck cancer | In vitro | EGCG induces apoptosis of cancer cells via regulating Bim and Bcl-2 | [119] |
Head and neck cancer | In vitro | Combined treatment with erlotinib and EGCG inhibited the protein level of p65 subunit of nuclear factor-kappaB | [120] |
Oral cancer | In vitro | EGCG inhibited cell viability in a time- and concentration-dependent manner | [122] |
Oral cancer | In vitro | Epigallocatechin-3-gallate in inhibiting HGF-induced tumor growth and invasion | [124] |
Oral cancer | In vitro | EGCG caused an inhibitory effect on cell migration, motility, spread, and adhesion | [125] |
Oesophagus cancer | In vitro | Epigallocatechin-3-gallate considerably reduced the invasion and viability capacity of cancer cells | [127] |
Oesophagus cancer | In vitro | Epigallocatechin-3-gallate inhibited proliferation of cancer cells | [128] |
Lymphoma | In vitro | Vorinostat alone or in combination with epigallocatechin-3-gallate imparts anti-proliferative effects | [130] |
Lymphoma | In vitro | EGCG-induced inhibition of tumor cell proliferation | [132] |
Lung cancer | In vitro | EGCG decrease the expression of both Axl and Tyro 3 receptor tyrosine kinases | [139] |
Myeloma | In vitro | The treatment of the cancer cell line with epigallocatechin-3-gallate inhibits cell proliferation as well induces apoptosis | [141] |
Myeloma | In vitro | EGCG inhibited the effect of endothelial cell migration induced and the numbers of migrated cells and numbers of migrated cells | [142] |
Osteosarcoma | In vitro | EGCG has an anticancer effect on cancer cells | [144] |
Osteosarcoma | In vitro | EGCG showed role in the suppression of proliferation of cancer cells in a concentration-dependent and time-dependent manner | [145] |
Brain tumor | In vitro | EGCG induced apoptosis in glioma cells. | [147] |
Brain tumor | In vitro | EGCG treatment leads to a decrease in cell viability and the S-phase cell fraction | [149] |
Thyroid cancer | In vitro | EGCG decreased the migration and invasion, | [151] |
Thyroid cancer | In vitro | EGCG considerably suppresses invasion and migration in anaplastic cancer cells | [152] |
Retinoblastoma | In vitro | EGCG treatment of cancer cells resulted in a dose- and time-dependent decrease in the total pRb | [154] |
EGCG + Anticancer Compound | Type of Cancer | Outcome of the Study | Refs. |
---|---|---|---|
EGCG + Doxorubicin | Osteosarcoma | Epigallocatechin-3-gallate reduce the Doxorubicin-induced pro-survival autophagy | [166] |
EGCG + Cisplatin or oxaliplatin | Colorectal cancer | Treatment of colorectal cancer cells with Epigallocatechin-3-gallate and cisplatin or oxaliplatin confirmed a synergistic effect on inhibition of cell proliferation and induction of cell death. | [167] |
EGCG + Sulindac | Intestinal nepoplasia | Treatment with both green tea extract and sulindac significantly decrease the number of per mouse | [168] |
EGCG + Celecoxib | Prostate cancer | Co-treatment with epigallocatechin-3-gallate and celecoxib powerfully induced the expression of both GADD153 mRNA level and protein | [169] |
EGCG + Sulforaphane | Ovarian cancer | Sulforaphane inhibits cell viability of cancer cell and epigallocatechin-3-gallate enhance the inhibiting effect of sulforaphane | [170] |
EGCG + Hydroxytamoxifen | Breast cancer | The combination of EGCG and 4-hydroxytamoxifen provokes synergistic cytotoxicity in cancer | [171] |
EGCG + Celecoxib | Pancreatic cancer | Co-incubation of cancer cells with celecoxib and epigallocatechin-3-gallate synergistically reduced metabolic activity through induction of apoptosis | [172] |
EGCG + SU5416 | Neuroblastoma | Combination of drugs can be a promising therapeutic strategy for controlling the growth of neuroblastoma cells. | [173] |
EGCG + Sulforaphane | Colon cancer | Low and high dose combinations of Sulforaphane and epigallocatechin-3-gallate attenuated the cellular senescence induced by epigallocatechin-3-gallate alone | [174] |
EGCG + Tamoxifen | Breast cancer | Tamoxifen at realistic dose suppress the growth of ER-negative breast cancer when combined with Epigallocatechin-3-gallate. | [175] |
EGCG + Taxane | Prostate cancer | Epigallocatechin-3-gallate in combination with taxane may provide a novel therapeutic treatment of prostate cancer | [176] |
EGCG + Doxorubicin | Prostate cancer | Epigallocatechin-3-gallate combined with Doxorubicin may have significant clinical application in the treatment of metastatic prostate cancer | [177] |
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Almatroodi, S.A.; Almatroudi, A.; Khan, A.A.; Alhumaydhi, F.A.; Alsahli, M.A.; Rahmani, A.H. Potential Therapeutic Targets of Epigallocatechin Gallate (EGCG), the Most Abundant Catechin in Green Tea, and Its Role in the Therapy of Various Types of Cancer. Molecules 2020, 25, 3146. https://doi.org/10.3390/molecules25143146
Almatroodi SA, Almatroudi A, Khan AA, Alhumaydhi FA, Alsahli MA, Rahmani AH. Potential Therapeutic Targets of Epigallocatechin Gallate (EGCG), the Most Abundant Catechin in Green Tea, and Its Role in the Therapy of Various Types of Cancer. Molecules. 2020; 25(14):3146. https://doi.org/10.3390/molecules25143146
Chicago/Turabian StyleAlmatroodi, Saleh A., Ahmad Almatroudi, Amjad Ali Khan, Fahad A. Alhumaydhi, Mohammed A. Alsahli, and Arshad Husain Rahmani. 2020. "Potential Therapeutic Targets of Epigallocatechin Gallate (EGCG), the Most Abundant Catechin in Green Tea, and Its Role in the Therapy of Various Types of Cancer" Molecules 25, no. 14: 3146. https://doi.org/10.3390/molecules25143146