Anticancer activities of epigallocatechin-3-gallate against cholangiocarcinoma cells

Kwak, Tae Won; Park, Su Bum; Kim, Hyun-Jung; Jeong, Young‐Il; Kang, Dae Hwan

doi:10.2147/ott.s112364

Cited by 51 publications

(28 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Generally, apoptosis is induced via two pathways, a cell death extrinsic pathway and a mitochondria‐dependent intrinsic pathway. Previous reports have concluded that EGCG induced caspase‐mediated apoptosis in several solid tumour cells, including chondrosarcoma, gastrointestinal stromal tumour, cholangiocarcinoma, esophageal cancer, pancreatic cancer and prostate cancer . EGCG also induced apoptosis in several types of leukaemia.…”

Section: Discussionmentioning

confidence: 95%

(−)‐Epigallocatechin‐3‐gallate induces cell apoptosis in chronic myeloid leukaemia by regulating Bcr/Abl‐mediated p38‐MAPK/JNK and JAK2/STAT3/AKT signalling pathways

Xiao

Jiang

et al. 2018

Clin Exp Pharma Physio

View full text Add to dashboard Cite

Summary Epigallocatechin‐3‐gallate (EGCG), a major polyphenolic constituent of green tea, possesses remarkable chemopreventive and therapeutic potential against various types of cancer, including leukaemia. However, the molecular mechanism involved in chronic myeloid leukaemia (CML), especially imatinib‐resistant CML cells, is not completely understood. In the present study, we investigated the effect of EGCG on the growth of Bcr/Abl+ CML cell lines, including imatinib‐resistant cell lines and primary CML cells. The results revealed that EGCG could inhibit cell growth and induce apoptosis in CML cells. The mechanisms involved inhibition of the Bcr/Abl oncoprotein and regulation of its downstream p38‐MAPK/JNK and JAK2/STAT3/AKT pathways. In conclusion, we documented the anti‐CML effects of EGCG in imatinib‐sensitive and imatinib‐resistant Bcr/Abl+ cells, especially T315I‐mutated cells.

show abstract

Section: Discussionmentioning

confidence: 95%

(−)‐Epigallocatechin‐3‐gallate induces cell apoptosis in chronic myeloid leukaemia by regulating Bcr/Abl‐mediated p38‐MAPK/JNK and JAK2/STAT3/AKT signalling pathways

Xiao

Jiang

et al. 2018

Clin Exp Pharma Physio

View full text Add to dashboard Cite

show abstract

“…19 EGCG also reported to initiate the mitochondrial pathway of apoptosis in different cancer cells [47][48][49] as well as in HeLa cells. 19 EGCG also reported to initiate the mitochondrial pathway of apoptosis in different cancer cells [47][48][49] as well as in HeLa cells.…”

Section: Discussionmentioning

confidence: 96%

Theaflavin and epigallocatechin‐3‐gallate synergistically induce apoptosis through inhibition of PI3K/Akt signaling upon depolymerizing microtubules in HeLa cells

Chakrabarty

Nag

Ganguli

et al. 2018

J of Cellular Biochemistry

View full text Add to dashboard Cite

Theaflavin (TF) and epigallocatechin‐3‐gallate (EGCG) both have been reported previously as microtubule depolymerizing agents that also have anticancer effects on various cancer cell lines and in animal models. Here, we have applied TF and EGCG in combination on HeLa cells to investigate if they can potentiate each other to improve their anticancer effect in lower doses and the underlying mechanism. We found that TF and EGCG acted synergistically, in lower doses, to inhibit the growth of HeLa cells. We found the combination of 50 µg/mL TF and 20 µg/mL EGCG to be the most effective combination with a combination index of 0.28. The same combination caused larger accumulation of cells in the G 2/M phase of the cell cycle, potent mitochondrial membrane potential loss, and synergistic augmentation of apoptosis. We have shown that synergistic activity might be due to stronger microtubule depolymerization by simultaneous binding of TF and EGCG at different sites on tubulin: TF binds at vinblastine binding site on tubulin, and EGCG binds near colchicines binding site on tubulin. A detailed mechanistic analysis revealed that stronger microtubule depolymerization caused effective downregulation of PI3K/Akt signaling and potently induced mitochondrial apoptotic signals, which ultimately resulted in the apoptotic death of HeLa cells in a synergistic manner.

show abstract

“…Tumor growth was significantly reduced in HuCC-T1 tumor-bearing mice subcutaneously injected with EGCG. Notch1 was found to be markedly reduced by EGCG treatment [51].…”

Section: Regulation Of Notch Pathwaymentioning

confidence: 90%

EGCG Mediated Targeting of Deregulated Signaling Pathways and Non-Coding RNAs in Different Cancers: Focus on JAK/STAT, Wnt/β-Catenin, TGF/SMAD, NOTCH, SHH/GLI, and TRAIL Mediated Signaling Pathways

Farooqi

Pinheiro

Granja

et al. 2020

Cancers

View full text Add to dashboard Cite

Decades of research have enabled us to develop a better and sharper understanding of multifaceted nature of cancer. Next-generation sequencing technologies have leveraged our existing knowledge related to intra- and inter-tumor heterogeneity to the next level. Functional genomics have opened new horizons to explore deregulated signaling pathways in different cancers. Therapeutic targeting of deregulated oncogenic signaling cascades by products obtained from natural sources has shown promising results. Epigallocatechin-3-gallate (EGCG) has emerged as a distinguished chemopreventive product because of its ability to regulate a myriad of oncogenic signaling pathways. Based on its scientifically approved anticancer activity and encouraging results obtained from preclinical trials, it is also being tested in various phases of clinical trials. A series of clinical trials associated with green tea extracts and EGCG are providing clues about significant potential of EGCG to mechanistically modulate wide ranging signal transduction cascades. In this review, we comprehensively analyzed regulation of JAK/STAT, Wnt/β-catenin, TGF/SMAD, SHH/GLI, NOTCH pathways by EGCG. We also discussed most recent evidence related to the ability of EGCG to modulate non-coding RNAs in different cancers. Methylation of the genome is also a widely studied mechanism and EGCG has been shown to modulate DNA methyltransferases (DNMTs) and protein enhancer of zeste-2 (EZH2) in multiple cancers. Moreover, the use of nanoformulations to increase the bioavailability and thus efficacy of EGCG will be also addressed. Better understanding of the pleiotropic abilities of EGCG to modulate intracellular pathways along with the development of effective EGCG delivery vehicles will be helpful in getting a step closer to individualized medicines.

show abstract

Anticancer activities of epigallocatechin-3-gallate against cholangiocarcinoma cells

Cited by 51 publications

References 32 publications

(−)‐Epigallocatechin‐3‐gallate induces cell apoptosis in chronic myeloid leukaemia by regulating Bcr/Abl‐mediated p38‐MAPK/JNK and JAK2/STAT3/AKT signalling pathways

(−)‐Epigallocatechin‐3‐gallate induces cell apoptosis in chronic myeloid leukaemia by regulating Bcr/Abl‐mediated p38‐MAPK/JNK and JAK2/STAT3/AKT signalling pathways

Theaflavin and epigallocatechin‐3‐gallate synergistically induce apoptosis through inhibition of PI3K/Akt signaling upon depolymerizing microtubules in HeLa cells

EGCG Mediated Targeting of Deregulated Signaling Pathways and Non-Coding RNAs in Different Cancers: Focus on JAK/STAT, Wnt/β-Catenin, TGF/SMAD, NOTCH, SHH/GLI, and TRAIL Mediated Signaling Pathways

Contact Info

Product

Resources

About