Tea Polyphenols Decrease Serum Levels of Prostate-Specific Antigen, Hepatocyte Growth Factor, and Vascular Endothelial Growth Factor in Prostate Cancer Patients and Inhibit Production of Hepatocyte Growth Factor and Vascular Endothelial Growth Factor <i>In vitro</i>

McLarty, Jerry; Bigelow, Rebecca L.; Smith, Mylinh; Elmajian, Don; Ankem, Murali K.; Cardelli, James A.

doi:10.1158/1940-6207.capr-08-0167

Cited by 229 publications

(181 citation statements)

References 61 publications

(85 reference statements)

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“…Polyphenol (-)-epigallocatechin-3-O-gallate (EGCG) inhibits the growth of tumor cells and induces apoptosis in cancer cells without adversely affecting normal cells (10)(11)(12), and several clinical trials have been carried out to evaluate its potential value as an anticancer agent (13)(14)(15)(16). 67LR has been identified as a cell surface EGCG target that is essential for the antitumor effect of EGCG in vivo (17,18).…”

Section: Introductionmentioning

confidence: 99%

67-kDa laminin receptor increases cGMP to induce cancer-selective apoptosis

Kumazoe

Sugihara²,

Tsukamoto³

et al. 2013

J. Clin. Invest.

111

215

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The 67-kDa laminin receptor (67LR) is a laminin-binding protein overexpressed in various types of cancer, including bile duct carcinoma, colorectal carcinoma, cervical cancer, and breast carcinoma. 67LR plays a vital role in growth and metastasis of tumor cells and resistance to chemotherapy. Here, we show that 67LR functions as a cancer-specific death receptor. In this cell death receptor pathway, cGMP initiated cancer-specific cell death by activating the PKCδ/acid sphingomyelinase (PKCδ/ASM) pathway. Furthermore, upregulation of cGMP was a rate-determining process of 67LR-dependent cell death induced by the green tea polyphenol (-)-epigallocatechin-3-O-gallate (EGCG), a natural ligand of 67LR. We found that phosphodiesterase 5 (PDE5), a negative regulator of cGMP, was abnormally expressed in multiple cancers and attenuated 67LR-mediated cell death. Vardenafil, a PDE5 inhibitor that is used to treat erectile dysfunction, significantly potentiated the EGCG-activated 67LR-dependent apoptosis without affecting normal cells and prolonged the survival time in a mouse xenograft model. These results suggest that PDE5 inhibitors could be used to elevate cGMP levels to induce 67LR-mediated, cancer-specific cell death.

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Section: Introductionmentioning

confidence: 99%

67-kDa laminin receptor increases cGMP to induce cancer-selective apoptosis

Kumazoe

Sugihara²,

Tsukamoto³

et al. 2013

J. Clin. Invest.

111

215

View full text Add to dashboard Cite

show abstract

“…Several clinical trials have been conducted to evaluate its potential role in cancer treatment (9)(10)(11). 67LR has been identified as a cell surface EGCG receptor that mediates an antitumor effect of EGCG in vivo (12,13).…”

Section: Introductionmentioning

confidence: 99%

Sphingosine Kinase-1 Protects Multiple Myeloma from Apoptosis Driven by Cancer-Specific Inhibition of RTKs

Tsukamoto

Huang

Kumazoe

et al. 2015

Molecular Cancer Therapeutics

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Activation of acid sphingomyelinase (ASM) leads to ceramide accumulation and induces apoptotic cell death in cancer cells. In the present study, we demonstrate that the activation of ASM by targeting cancer-overexpressed 67-kDa laminin receptors (67LR) induces lipid raft disruption and inhibits receptor tyrosine kinase (RTK) activation in multiple myeloma cells. Sphingosine kinase 1 (SphK1), a negative regulator of ceramide accumulation with antiapoptotic effects, was markedly elevated in multiple myeloma cells. The silencing of SphK1 potentiated the apoptotic effects of the green tea polyphenol epigallocatechin-3-O-gallate (EGCG), an activator of ASM through 67LR. Furthermore, the SphK1 inhibitor safingol synergistically sensitized EGCG-induced proapoptotic cell death and tumor suppression in multiple myeloma cells by promoting the prevention of RTK phosphorylation and activation of death-associated protein kinase 1 (DAPK1). We propose that targeting 67LR/ASM and SphK1 may represent a novel therapeutic strategy against multiple myeloma.

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“…Following-up of the participants as a long-term research revealed that continued inhibition of development of prostate cancer from PIN even two years after initial treatment with GTCs [98]. These observations appear to provide evidence of the beneficial efficacies of GTCs on the prevention of human malignancies, although three other interventional studies investigating the effect of green tea against prostate cancer found no beneficial effects [99][100][101]. These three studies with negative results include patients with established malignancies of prostate, while only patients with pre-malignant lesions participate in the trial conducted by Bettuzzi et al [97,98].…”

Section: Clinical Interventional Studiesmentioning

confidence: 96%

Dietary Phytochemicals as Cancer Preventive Agents: Efficacy and Mechanisms

Sakai¹

2015

J Bioanal Biomed

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Despite significant advances in cancer therapeutic modalities, available anti-tumor drugs display limited efficacy and sometimes carry a risk of severe adverse side effect. Therefore, it is important to identify and develop cancer chemopreventive agents without toxicity. Epidemiological examinations in human populations and experimental rodent studies provide evidence that certain types of phytochemicals suppress development and growth of cancers at various organ sites. A number of clinical investigations have been also conducted and shown that dietary phytochemicals are able to inhibit tumorigenesis, indicating several phytochemicals are regarded as cancer chemopreventive agents. Epigallocatechin-3-gallate (EGCG), the major catechin in green tea, is considered as the most biologically active constituent in drinking tea with respect to inhibiting cell proliferation and inducing apoptosis in cancer cells. EGCG appears to directly target receptor tyrosine kinases with inhibiting activation of the receptors and down-stream signaling pathways. In addition, EGCG has improving effects against obesity and insulin resistance, which leads to suppressing the development of obesity-related malignancies. Other polyphenolic phytochemicals, including curcumin and resveratrol, are also reported to exert anti-cancer effect. In this review article, we summarize the potential of dietary phytochemicals as anti-cancer drugs and those possible mechanisms against cancer, especially chemopreventive effect of green tea catechins.

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Tea Polyphenols Decrease Serum Levels of Prostate-Specific Antigen, Hepatocyte Growth Factor, and Vascular Endothelial Growth Factor in Prostate Cancer Patients and Inhibit Production of Hepatocyte Growth Factor and Vascular Endothelial Growth Factor In vitro

Cited by 229 publications

References 61 publications

67-kDa laminin receptor increases cGMP to induce cancer-selective apoptosis

67-kDa laminin receptor increases cGMP to induce cancer-selective apoptosis

Sphingosine Kinase-1 Protects Multiple Myeloma from Apoptosis Driven by Cancer-Specific Inhibition of RTKs

Dietary Phytochemicals as Cancer Preventive Agents: Efficacy and Mechanisms

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