Epigallocatechin-3-Gallate: The Prospective Targeting of Cancer Stem Cells and Preventing Metastasis of Chemically-Induced Mammary Cancer in Rats

El-Rahman, Sahar S. Abd; Shehab, Gehan G.; Nashaat, Heba

doi:10.1016/j.amjms.2017.03.001

Cited by 18 publications

(8 citation statements)

References 37 publications

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“…In conclusion, while three-dimensional spheroids assays are commonly used to uncover more relevant ovarian tumor biology than classical culture conditions, one must acknowledge that such assays at this stage may still preclude direct clinical application. Interestingly, our study supports the impact of EGCG as a prospective targeting of CSC and in the potential prevention of metastasis in a pre-clinical in vivo study of chemically-induced mammary cancer in rats [ 67 ]. Here, our work highlights and supports the chemopreventive benefits of the diet-derived EGCG and its capacity to target intracellular transducing events that regulate the acquisition of an invasive ovarian CSC phenotype.…”

Section: Discussionsupporting

confidence: 77%

Epigallocatechin-3-Gallate Prevents the Acquisition of a Cancer Stem Cell Phenotype in Ovarian Cancer Tumorspheres through the Inhibition of Src/JAK/STAT3 Signaling

et al. 2023

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Three-dimensional tumorsphere cultures recapitulate the expression of several cancer stem cell (CSC) biomarkers and represent an effective in vitro platform to screen the anti-CSC properties of drugs. Whereas ovarian carcinoma is among the leading causes of death for women, ovarian CSC (OvCSC), a highly malignant subpopulation of ovarian cancer cells, is thought to be responsible for therapy resistance, metastasis, and tumor relapse. Epigallocatechin-3-gallate (EGCG), a diet-derived active polyphenol found in green tea leaves, can suppress ovarian cancer cell proliferation and induce apoptosis. However, its capacity to prevent the acquisition of cancer stemness traits in ovarian malignancies remains unclear. Here, we exploited the in vitro three-dimensional tumorsphere culture model to explore the capacity of EGCG to alter CSC biomarkers expression, signal transducing events and cell chemotaxis. Total RNA and protein lysates were isolated from human ES-2 ovarian cancer cell tumorspheres for gene assessment by RT-qPCR and protein expression by immunoblot. Real-time cell chemotaxis was assessed with xCELLigence. Compared with their parental adherent cells, tumorspheres expressed increased levels of the CSC markers NANOG, SOX2, PROM1, and Fibronectin. EGCG treatment reduced dose-dependently tumorspheres size and inhibited the transcriptional regulation of those genes. Src and JAK/STAT3 signaling pathways appeared to be relevant for CSC phenotype and chemotactic response. In conclusion, these data highlight and support the chemopreventive benefits of the diet-derived EGCG and its capacity to target intracellular transducing events that regulate the acquisition of an invasive CSC phenotype.

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Section: Discussionsupporting

confidence: 77%

Epigallocatechin-3-Gallate Prevents the Acquisition of a Cancer Stem Cell Phenotype in Ovarian Cancer Tumorspheres through the Inhibition of Src/JAK/STAT3 Signaling

et al. 2023

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“…In addition, the tumor vasculature is the major route of metastasis of cancer cells from the primary site to distant organs. Anti-angiogenic effects of a variety of phytochemicals have been demonstrated in various cancer cells in vitro as well as using in vivo tumor models [5][6][7]. The anti-angiogenic effect of gallic acid Ivyspring International Publisher in ovarian cancer is due to the downregulation of the Phosphatase and tensin homologue deleted on chromosome 10/Protein kinase B/Hypoxia-inducible factor-1alpha (PTEN/AKT/HIF-1α) pathway and inhibition of vascular endothelial growth factor (VEGF) expression [8].…”

Section: Introductionmentioning

confidence: 99%

Naringenin exerts anticancer effects by inducing tumor cell death and inhibiting angiogenesis in malignant melanoma

Choi¹,

Lee²,

Jang³

et al. 2020

Int. J. Med. Sci.

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Malignant melanoma is one of the most deadly skin cancer, due to its aggressive proliferation and metastasis. Naringenin, abundantly present in citrus fruits, has widely studied in cancer therapy. In this study, we investigated whether naringenin also has anticancer effects against B16F10 murine and SK-MEL-28 human melanoma cells. Moreover, we assessed the effects of naringenin treatment on angiogenesis of HUVECs and ex vivo sprouting of microvessels.Naringenin inhibited tumor cell proliferation and migration in a dose-dependent manner in B16F10 and SK-MEL-28 cells, which is supported by the results that phosphorylation of ERK1/2 and JNK MAPK decreased. Furthermore, naringenin induced cell apoptosis. Western blot analysisshowed naringenin treatment significantly upregulated the protein expression of activated cas3 and PARP in B16F10 and SK-MEL-28 cells. In addition, in vitro and ex vivo angiogenesis assays demonstrated that naringenin treatment potently suppressed EC migration, tube formation, and sprouting of microvessels. RT-PCR analysis showed that naringenin treatment significantly reduced the mRNA expression of Tie2, but did not inhibit the expression of Ang2. In conclusion, present study demonstrates the anticancer effects of naringenin by its induction of tumor cell death and inhibition of angiogenesis in malignant melanoma, suggesting that naringenin has potential as a safe and effective therapeutic agent to treat melanoma.

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“…In clinical anti-angiogenic therapy, bevacizumab (Avastin) is a monoclonal antibody for anti-vascular endothelial growth factor (VEGF) that counteracts the action of VEGF and inhibits tumor angiogenesis (7,8). Numerous phytochemicals, such as curcumin or epigallocatechin-3-gallate (EGCG) have been demonstrated to exert anti-angiogenic bioactivities in several in vitro and in vivo models (9)(10)(11). Thus, identification of phytochemicals with non-cytotoxic effects on normal cells and effective anti-angiogenic action could be of great clinical significance (11)(12)(13).…”

Section: Introductionmentioning

confidence: 99%

Kaempferol inhibits angiogenic ability by targeting VEGF receptor-2 and downregulating the PI3K/AKT, MEK and ERK pathways in VEGF-stimulated human umbilical vein endothelial cells

et al. 2018

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Anti-angiogenesis is one of the most general clinical obstacles in cancer chemotherapy. Kaempferol is a flavonoid phytochemical found in many fruits and vegetables. Our previous study revealed that kaempferol triggered apoptosis in human umbilical vein endothelial cells (HUVECs) by ROS‑mediated p53/ATM/death receptor signaling. However, the anti‑angiogenic potential of kaempferol remains unclear and its underlying mechanism warranted further exploration in VEGF‑stimulated HUVECs. In the present study, kaempferol significantly reduced VEGF‑stimulated HUVEC viability. Kaempferol treatment also inhibited cell migration, invasion, and tube formation in VEGF‑stimulated HUVECs. VEGF receptor‑2 (VEGFR‑2), and its downstream signaling cascades (such as AKT, mTOR and MEK1/2‑ERK1/2) were reduced as determined by western blotting and kinase activity assay in VEGF‑stimulated HUVECs after treatment with kaempferol. The present study revealed that kaempferol may possess angiogenic inhibition through regulation of VEGF/VEGFR‑2 and its downstream signaling cascades (PI3K/AKT, MEK and ERK) in VEGF-stimulated endothelial cells.

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Epigallocatechin-3-Gallate: The Prospective Targeting of Cancer Stem Cells and Preventing Metastasis of Chemically-Induced Mammary Cancer in Rats

Cited by 18 publications

References 37 publications

Epigallocatechin-3-Gallate Prevents the Acquisition of a Cancer Stem Cell Phenotype in Ovarian Cancer Tumorspheres through the Inhibition of Src/JAK/STAT3 Signaling

Epigallocatechin-3-Gallate Prevents the Acquisition of a Cancer Stem Cell Phenotype in Ovarian Cancer Tumorspheres through the Inhibition of Src/JAK/STAT3 Signaling

Naringenin exerts anticancer effects by inducing tumor cell death and inhibiting angiogenesis in malignant melanoma

Kaempferol inhibits angiogenic ability by targeting VEGF receptor-2 and downregulating the PI3K/AKT, MEK and ERK pathways in VEGF-stimulated human umbilical vein endothelial cells

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