Epigallocatechin-3-Gallate (EGCG) Suppresses Pancreatic Cancer Cell Growth, Invasion, and Migration partly through the Inhibition of Akt Pathway and Epithelial–Mesenchymal Transition: Enhanced Efficacy When Combined with Gemcitabine
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Most pancreatic cancers are usually diagnosed at an advanced stage when they have already metastasized. Epigallocatechin-3-gallate (EGCG), a major polyphenolic constituent of green tea, has been shown to reduce pancreatic cancer growth, but its effect on metastasis remains elusive. This study evaluated the capacity of EGCG to inhibit pancreatic cancer cell migration and invasion and the underlying mechanisms. EGCG reduced pancreatic cancer cell growth, migration, and invasion in vitro and in vivo. EGCG prevented “Cadherin switch” and decreased the expression level of TCF8/ZEB1, β-Catenin, and Vimentin. Mechanistically, EGCG inhibited the Akt pathway in a time-dependent manner, by suppressing IGFR phosphorylation and inducing Akt degradation. Co-treatment with catalase or N-Acetyl-L-cysteine did not abrogate EGCG’s effect on the Akt pathway or cell growth. Moreover, EGCG synergized with gemcitabine to suppress pancreatic cancer cell growth, migration, and invasion, through modulating epithelial–mesenchymal transition markers and inhibiting Akt pathway. In summary, EGCG may prove beneficial to improve gemcitabine sensitivity in inhibiting pancreatic cancer cell migration and invasion, to some extent through the inhibition of Akt pathway and epithelial–mesenchymal transition.
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EGCG inhibits the initiation, promotion, and progression of different types of tumors in vitro and in vivo.
“Numerous studies, both in vitro using various cancer cell lines and in vivo in animal models, have consistently demonstrated the ability of EGCG to inhibit the initiation, promotion, and progression of different types of tumors.141–145”
From Drug repurposing for cancer therapy (2024) · cites this paper as [145]
The Introduction says EGCG has preventive and therapeutic properties in various cancer models, and the Discussion reports reduced pancreatic tumor growth in vitro and in vivo. The paper does not establish inhibition at each of the specified stages—initiation, promotion, and progression—across different tumor types. (LLM, conf=0.85)
Experimental — accuracy not yet measuredEGCG reduces mRNA expression and transcriptional activity of β-catenin in wild-type P53-expressing KB cells.
“another study found that EGCG was involved in reducing the mRNA expression and transcriptional activity of β-catenin in wild-type P53-expressing KB cells.”
From Drug repurposing for cancer therapy (2024) · cites this paper as [145]
The Discussion (section 4; page unavailable) says EGCG downregulated β-catenin expression in pancreatic cancer cells and mouse xenografts. It does not report reduced β-catenin mRNA or transcriptional activity in wild-type P53-expressing KB cells; the qRT-PCR methods (section 2.9; page unavailable) describe measuring Akt mRNA instead. (LLM, conf=0.88)
Experimental — accuracy not yet measuredEGCG used in combination with gemcitabine exerts stronger inhibitory effects on β-catenin and N-cadherin in pancreatic cancer cells.
“When used in combination with gemcitabine, EGCG was found to exert stronger inhibitory effects on β-catenin and N-cadherin in pancreatic cancer cells.145”
From Drug repurposing for cancer therapy (2024) · cites this paper as [145]
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- Authors
- Wei, R., Cortez Penso, N. E., Hackman, R. M., Wang, Y., & Mackenzie, G. G.
- Affiliations
- Zhejiang University (CN)
- Department of Nutrition, University of California, Davis, CA 95616, USA
- University of California, Davis (US)
- Corresponding author
- Wang, Yuefei
- Mackenzie, Gerardo G.
- Venue
- Nutrients
- Publisher
- MDPI AG
- Published
- 2019-08-09
- Volume
- 11
- Issue
- 8
- Pages
- 1856
- ISSN
- 2072-6643 (ISSN-L)
- PMC
- PMC6722696
- OpenAlex
- W2968952801
- Cited by
- 78
- References
- 39
- Citations by year
- 2026: 10 · 2025: 8 · 2024: 7 · 2023: 15 · 2022: 7 · 2021: 18 · 2020: 11 · 2019: 2
- FWCI
- 6.99
- Type
- journal article
- Language
- en
- Open access
- gold
- dx.doi.org
- Licence
- Locations
- Nutrients (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- eScholarship (California Digital Library) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- China Scholarship Council
- University of California, Davis (P30CA093373, NCI P30CA093373)
- National Cancer Institute (NCI P30 CA093373, P30CA093373)
- Comprehensive Cancer Center, University of California, Davis (NCI P30CA093373, P30CA093373)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Tea Polyphenols and Effects
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Keywords
- epigallocatechin gallate, pancreatic cancer, Akt signaling, epithelial-mesenchymal transition, cell migration, cell invasion, gemcitabine combination therapy, ZEB1, β-catenin, green tea polyphenols, metastasis
- MeSH terms
- Gemcitabine, Animals, Antineoplastic Combined Chemotherapy Protocols, Catechin, Cell Movement, Deoxycytidine, Enzyme Stability, Humans, Mice, Inbred C57BL, Neoplasm Invasiveness, Pancreatic Neoplasms, Signal Transduction, Cell Line, Tumor, Tumor Burden, Cell Proliferation, Proto-Oncogene Proteins c-akt, Epithelial-Mesenchymal Transition, Proteolysis
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