Epigallocatechin-3-gallate inhibits cell growth, induces apoptosis and causes S phase arrest in hepatocellular carcinoma by suppressing the AKT pathway

Shen, Xiaofeng; Zhang, Yong; Yan, Feng; Zhang, Litu; Li, Jilin; Xie, Yuan; Luo, Xi

doi:10.3892/ijo.2014.2251

Cited by 55 publications

(32 citation statements)

References 31 publications

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“…For instance, EGCG has attracted growing attention due to its low toxicity in normal cells and significant inhibitory effect on cancer cells (26,27). Our previous research demonstrated that EGCG significantly inhibits the growth of hepatocellular carcinoma cells SMMC7721 at 48 h (28). In this study, we assessed the apoptotic effects of EGCG in B lymphoma cells and investigated the possible molecular mechanisms.…”

Section: Discussionmentioning

confidence: 99%

(−)-Epigallocatechingallate induces apoptosis in B lymphoma cells via caspase-dependent pathway and Bcl-2 family protein modulation

Wang

Xie

Yan

et al. 2015

International Journal of Oncology

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(−)-Epigallocatechingallate (EGCG) as a representative polyphenol has attracted increasing attention due to its diversified effects, especially its potential as an agent for the prevention or treatment of certain cancers. However, the molecular mechanisms of EGCG-induced apoptosis in B lymphoma cells are unclear. The aim of this study was to investigate the effect of EGCG on proliferation and apoptosis in the B lymphoma cell lines Jeko-1 and Raji, and determine the underlying mechanisms. Cell proliferation and cytotoxicity were determined by the cell counting kit (CCK-8) assay; apoptosis was assessed by flow cytometry using the Annexin V-PE/7AAD double staining; Fas, Bcl-2 and Bax mRNA expression levels were determined by real-time PCR; caspase activity was measured by the caspase activity assay kit; the expression levels of apoptosis-associated proteins were determined by western blot analysis. We demonstrated that EGCG induced growth inhibition and apoptosis in a dose- and time-dependent manner. In agreement, EGCG upregulated the mRNA expression of Fas and Bax while downregulating Bcl-2. Protein expression levels of Bax, activated caspase-3, -7, -8, and -9, and PARP were increased, while Bcl-2 protein levels were reduced by EGCG treatment. Taken together, EGCG induces B lymphoma cell apoptosis by triggering caspase-dependent intrinsic (mitochondrial) and extrinsic (death receptor) pathways. These findings suggest that EGCG may be a potential agent for the treatment of B lymphoma.

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Section: Discussionmentioning

confidence: 99%

(−)-Epigallocatechingallate induces apoptosis in B lymphoma cells via caspase-dependent pathway and Bcl-2 family protein modulation

Wang

Xie

Yan

et al. 2015

International Journal of Oncology

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“…Among the class of secondary metabolites, flavonoids stand out as efflux pump inhibitors particularly because they inhibit P-gp ATP-ase activity by interacting with the ATP-binding sites [62, 63]. The natural product polyphenol epigallocatechin-3-gallate (EGCG), the most abundant and active phenolic compound found in green tea, exhibits antitumor properties [64-66]. Numerous studies have demonstrated that EGCG affects many signaling pathways including Janus kinase (JAK)/signal transducer and activator of transcription (STAT), mitogen-activated protein kinases (MAPK), phosphoinositide 3-kinase (PI3K/AKT), WNT, Hedgehog (Hh) and NOTCH [67, 68].…”

Section: Phytometabolites Targeting Cscs Modulate Abc Transporters Kmentioning

confidence: 99%

Anti-Cancer Phytometabolites Targeting Cancer Stem Cells

Torquato

Goettert²,

Justo³

et al. 2017

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Medicinal plants are a plentiful source of bioactive molecules with much structural diversity. In cancer treatment, molecules obtained from plants represent an attractive alternative to other treatments because several plant-derived compounds have exhibited lower toxicity and higher selectivity against cancer cells. In this review, we focus on the possible application of bioactive molecules obtained from plants against more primitive cell populations in cancers, cancer stem cells. Cancer stem cells are present in several kinds of tumors and are responsible for recurrences and metastases. Common anti-cancer drugs exhibit lower effectiveness against cancer stem cells because of their biological features. However, recently discovered natural phytometabolites exert cytotoxic effects on this rare population of cells in cancers. Therefore, this review presents the latest research on promising compounds from plants that can act as antitumor drugs and that mainly affect stem cell populations in cancers.

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“…Noh et al showed that EGCG improves Dermatophagoides pteronissinus extract-induced atopic dermatitis-like skin lesions in a mouse model by suppressing MIF [437]. In addition, EGCG can inhibit TNF-α [438], iNOS [439, 440], AKT [441], the CXC group of cytokines [442], and by by reducing the transcriptional activity of NF-κB, COX-2 expression and PGE-2 synthesis [443–448]. Additionally, EGCG activates wild-type p53 [449–451], and protects from p53 mutation [452].…”

Section: Low Toxicity Approachesmentioning

confidence: 99%

A multi-targeted approach to suppress tumor-promoting inflammation

Samadi

Bilsland

Georgakilas

et al. 2015

Seminars in Cancer Biology

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Cancers harbor significant genetic heterogeneity and patterns of relapse following many therapies are due to evolved resistance to treatment. While efforts have been made to combine targeted therapies, significant levels of toxicity have stymied efforts to effectively treat cancer with multi-drug combinations using currently approved therapeutics. We discuss the relationship between tumor-promoting inflammation and cancer as part of a larger effort to develop a broad-spectrum therapeutic approach aimed at a wide range of targets to address this heterogeneity. Specifically, macrophage migration inhibitory factor, cyclooxygenase-2, transcription factor nuclear factor-kappaB, tumor necrosis factor alpha, inducible nitric oxide synthase, protein kinase B, and CXC chemokines are reviewed as important antiinflammatory targets while curcumin, resveratrol, epigallocatechin gallate, genistein, lycopene, and anthocyanins are reviewed as low-cost, low toxicity means by which these targets might all be reached simultaneously. Future translational work will need to assess the resulting synergies of rationally designed antiinflammatory mixtures (employing low-toxicity constituents), and then combine this with similar approaches targeting the most important pathways across the range of cancer hallmark phenotypes.

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Epigallocatechin-3-gallate inhibits cell growth, induces apoptosis and causes S phase arrest in hepatocellular carcinoma by suppressing the AKT pathway

Cited by 55 publications

References 31 publications

(−)-Epigallocatechingallate induces apoptosis in B lymphoma cells via caspase-dependent pathway and Bcl-2 family protein modulation

(−)-Epigallocatechingallate induces apoptosis in B lymphoma cells via caspase-dependent pathway and Bcl-2 family protein modulation

Anti-Cancer Phytometabolites Targeting Cancer Stem Cells

A multi-targeted approach to suppress tumor-promoting inflammation

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