Molecular mechanism of epigallocatechin-3-gallate in human esophageal squamous cell carcinoma in vitro and in vivo

Liu, Lifeng; Hou, Ling; Gu, Shanzhi; Zuo, Xianbo; Du, Min; Luo, Min; Zhang, Xiaojin; Huang, Shangke; Zhao, Xinhan

doi:10.3892/or.2014.3555

Cited by 30 publications

(22 citation statements)

References 39 publications

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“…In addition, these polyphenols modulate the functions of various cancer-related signaling molecules. For example, the function and expression of vascular endothelial growth factor (VEGF), which is a strong stimulator of angiogenesis, are mediated by GTPs in oral cancer and esophageal squamous cell carcinoma [ 14 , 29 ]. Furthermore, in these malignancies, cyclin D1, which is a cell cycle regulator, and caspase-3, which is an important determinant for apoptosis, are associated with GTPs [ 14 , 29 ].…”

Section: Anticancer Effects Of Green Tea Polyphenolsmentioning

confidence: 99%

Anticancer Effects of Green Tea and the Underlying Molecular Mechanisms in Bladder Cancer

et al. 2018

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Green tea and green tea polyphenols (GTPs) are reported to inhibit carcinogenesis and malignant behavior in several diseases. Various in vivo and in vitro studies have shown that GTPs suppress the incidence and development of bladder cancer. However, at present, opinions concerning the anticancer effects and preventive role of green tea are conflicting. In addition, the detailed molecular mechanisms underlying the anticancer effects of green tea in bladder cancer remain unclear, as these effects are regulated by several cancer-related factors. A detailed understanding of the pathological roles and regulatory mechanisms at the molecular level is necessary for advancing treatment strategies based on green tea consumption for patients with bladder cancer. In this review, we discuss the anticancer effects of GTPs on the basis of data presented in in vitro studies in bladder cancer cell lines and in vivo studies using animal models, as well as new treatment strategies for patients with bladder cancer, based on green tea consumption. Finally, on the basis of the accumulated data and the main findings, we discuss the potential usefulness of green tea as an antibladder cancer agent and the future direction of green tea-based treatment strategies for these patients.

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Section: Anticancer Effects Of Green Tea Polyphenolsmentioning

confidence: 99%

Anticancer Effects of Green Tea and the Underlying Molecular Mechanisms in Bladder Cancer

et al. 2018

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“…sinensis . Epidemiological studies and murine models have identified promising results for green tea and its constituents in reducing the risk of cancer in different organs 8 – 11 . Green tea inhibited tumor growth in xenograft models by suppressing the metastasis on metastasis-specific mouse mammary carcinoma 4T1 cells 12 .…”

Section: Introductionmentioning

confidence: 99%

“…Green tea inhibited tumor growth in xenograft models by suppressing the metastasis on metastasis-specific mouse mammary carcinoma 4T1 cells 12 . In addition, epigallocatechin-3-gallate (EGCG), the major polyphenol of green tea, has been shown to inhibit proliferation and induce apoptosis through caspase-3 activation and to decrease VEGF expression in esophageal squamous cell carcinoma in vitro and in vivo 8 , 13 .…”

Section: Introductionmentioning

confidence: 99%

Antitumor activities of Quercetin and Green Tea in xenografts of human leukemia HL60 cells

Calgarotto

Maso

Franchi

et al. 2018

Sci Rep

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Quercetin is one of the most abundant flavonoids, present in fruits and vegetables and has been shown to have multiple properties capable of reducing cell growth in cancer cells. Green tea is a widely consumed beverage, known for a potential source of free radical scavenging and anti-cancer activities. Herein, we investigate the in vivo antitumor efficacy of quercetin and green tea in human leukemia. Human tumors were xenografted into NOD/SCID mice. Quercetin and green tea reduced tumor growth in HL-60 xenografts accompanied by decreased expression of anti-apoptotic proteins, BCL-2, BCL-XL and MCL-1 and increased expression of BAX, a pro-apoptotic protein. Moreover, caspase-3 was activated to a greater extent after quercetin and green tea treatment. Quercetin and green tea also mediated G1 phase cell cycle arrest in HL-60 xenografts. Treatment with quercetin and green tea induced conversion of LC3-I to LC3-II as well as activation of autophagy proteins, suggesting that quercetin and green tea initiate the autophagic progression. We have provided evidence that quercetin and green tea induces signaling at the level of apoptosis, cell cycle and autophagy which converge to antigrowth effects in HL-60 xenograft mice suggesting that these compounds may be a compelling ally in cancer treatment.

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“…BaP promoted significant G2/M arrest, and it is widely accepted that BaP exposure can cause DNA damage, so G2/M arrest allows for DNA repair prior to mitosis to prevent the propagation of mutated cells . Either G1 or G2/M arrest induction upon EGCG treatment has been observed in esophageal and lung cancer cell lines. Cells co‐treated with BaP and EGCG had a significant induction of ROS compared with the BaP‐treated cells after 2, 4, and 8 h. Hwang et al found that colon cancer cells treated with EGCG for 6 h induced ROS formation, so the same phenomena could have occurred in this study .…”

Section: Discussionmentioning

confidence: 99%

Epigallocatechin‐3‐gallate augments the therapeutic effects of benzo[a]pyrene‐mediated lung carcinogenesis

2017

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Our previous study found curcumin and vitamin E to have protective effects against benzo[a]pyrene (BaP) exposure in human normal lung epithelial BEAS-2B cells. The first objective of the present study was to determine whether epigallocatechin-3-gallate (EGCG) elicited the same response. Co-treatment with 5 μM BaP and 20 μM EGCG in BEAS-2B promoted a significant reduction in cell viability and greater G2/M cell cycle arrest, induction of ROS, and reductions in BaP-induced CYP1A1/CYP1B1/COMT, EGFR, p-Akt (Ser473), p-p53 (Thr55), and survivin mRNA/protein expression, as well as an increase in p-p53 (Ser15). Based on these findings, the second objective was to extend the investigation by developing a novel BaP-transformed BEAS-2B cell line, BEAS-2BBaP, to examine the effects of EGCG when co-administered with gefitinib, an EGFR tyrosine kinase inhibitor. Cell colony formation assay demonstrated in vitro tumorigenic potential of BEAS-2BBaP, which had an overexpression of EGFR. Viability testing revealed gefitinib co-treatment with EGCG resulted in more cell death compared to gefitinib alone. Co-treated cells had greater reductions in gefitinib-induced CYP1A1/CYB1B1, EGFR, cyclin D1, p-Akt (Ser473), and survivin mRNA/protein expression, as well as an increase in p-p53 (Ser15). Therefore, EGCG was found to promote greater cytotoxicity to BEAS-2B co-treated with BaP and BEAS-2BBaP upon gefitinib co-treatment through regulating metabolism enzymes and signaling pathways involving EGFR and p53. These findings suggest that EGCG did not act as a protective compound in BEAS-2B after acute BaP exposure, but has the potential to be a useful adjuvant chemotherapeutic compound when coupled with gefitinib for chemosensitization.

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Molecular mechanism of epigallocatechin-3-gallate in human esophageal squamous cell carcinoma in vitro and in vivo

Cited by 30 publications

References 39 publications

Anticancer Effects of Green Tea and the Underlying Molecular Mechanisms in Bladder Cancer

Anticancer Effects of Green Tea and the Underlying Molecular Mechanisms in Bladder Cancer

Antitumor activities of Quercetin and Green Tea in xenografts of human leukemia HL60 cells

Epigallocatechin‐3‐gallate augments the therapeutic effects of benzo[a]pyrene‐mediated lung carcinogenesis

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