Dose dependent effects of cadmium on tumor angiogenesis

Wei, Tianshu; Jia, Jin; Wada, Youichiro; Kapron, Carolyn M.; Liu, Ju

doi:10.18632/oncotarget.16572

Cited by 41 publications

(33 citation statements)

References 136 publications

(385 reference statements)

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“…With respect to plausible biological mechanisms that could explain the observed inverse associations, it has been reported that the effects of cadmium on tumor angiogenesis in breast cancer cells and other tumor models, can be either stimulatory or inhibitory, depending on the concentrations. 42,43 Ultra-low concentrations of cadmium (<0.5 μM) inhibit endothelial nitric oxide synthase (eNOS) activation, leading to reduced eNOS production and attenuated tumor angiogenesis. 44 Additionally, cadmium in high concentrations (>10 μM) induces both endothelial cells apoptosis via the activation of caspase-3, resulting in destruction of tumor vasculature.…”

Section: Discussionmentioning

confidence: 99%

Chronic long‐term exposure to cadmium air pollution and breast cancer risk in the French E3N cohort

Amadou

Praud

Coudon

et al. 2019

Intl Journal of Cancer

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Cadmium, due to its estrogen‐like activity, has been suspected to increase the risk of breast cancer; however, epidemiological studies have reported inconsistent findings. We conducted a case–control study (4,059 cases and 4,059 matched controls) nested within the E3N French cohort study to estimate the risk of breast cancer associated with long‐term exposure to airborne cadmium pollution, and its effect according to molecular subtype of breast cancer (estrogen receptor negative/positive [ER−/ER+] and progesterone receptor negative/positive [PR−/PR+]). Atmospheric exposure to cadmium was assessed using a Geographic Information System‐based metric, which included subject's residence‐to‐cadmium source distance, wind direction, exposure duration and stack height. Adjusted odds ratios (OR) and 95% confidence intervals (CI) were estimated using conditional logistic regression. Overall, there was no significant association between cumulative dose of airborne cadmium exposure and the risk of overall, premenopausal and postmenopausal breast cancer. However, by ER and PR status, inverse associations were observed for ER− (ORQ5 vs. Q1 = 0.63; 95% CI: 0.41–0.95, ptrend = 0.043) and for ER−/PR− breast tumors (ORQ4 vs. Q1 = 0.62; 95% CI: 0.40–0.95, ORQ5 vs. Q1 = 0.68; 95% CI: 0.42–1.07, ptrend = 0.088). Our study provides no evidence of an association between exposure to cadmium and risk of breast cancer overall but suggests that cadmium might be related to a decreased risk of ER− and ER−/PR− breast tumors. These observations and other possible effects linked to hormone receptor status warrant further investigations.

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Section: Discussionmentioning

confidence: 99%

Chronic long‐term exposure to cadmium air pollution and breast cancer risk in the French E3N cohort

Amadou

Praud

Coudon

et al. 2019

Intl Journal of Cancer

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“…The current study is the first, to our knowledge, to provide evidence for the effect of Cd on CFH expression and production in glomeruli, suggesting Cd as a crucial regulator of the innate immune system. Cd affects multiple organs, including liver and kidney, and the vascular system is also one of the primary targets of Cd-induced toxicity (42,43). At lower concentrations, Cd does not induce cytotoxicity in endothelial cells (7,9,44) but increases expression of vascular hemostastic factors, such as tissue factor and von Willebrand factor (45).…”

Section: Discussionmentioning

confidence: 99%

Cadmium Induces Glomerular Endothelial Cell–Specific Expression of Complement Factor H via the −1635 AP-1 Binding Site

Chen

Liu

et al. 2019

The Journal of Immunology

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Cadmium (Cd) is an environmental toxin that induces nephrotoxicity. Complement factor H (CFH), an inhibitor of complement activation, is involved in the pathogenesis of various renal diseases. In this study, we investigated the effects of Cd on CFH production by the kidney. In C57B6/J mice, an increased CFH level was found in renal blood and glomerular endothelial cells after Cd treatment. In vitro, Cd induces an increased CFH secretion and mRNA expression in human renal glomerular endothelial cells but not in human podocytes or human mesangial cells. Cd activates the JNK pathway and increases c-Jun and c-Fos in human renal glomerular endothelial cells. A JNK inhibitor, SP600125, specifically abolishes Cd-induced CFH production. By chromatin immunoprecipitation assay and EMSA, the −1635 AP-1 motif on human CFH promoter was identified as the binding element for c-Jun and c-Fos. In a luciferase activity assay, mutation of the AP1 site eliminates Cd-induced increase of CFH promoter activity. Thus, the −1635 AP-1 motif on the CFH promoter region mediates Cd-inducible CFH gene expression.

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“…Inhibition of angiogenesis has thus been regarded as a valuable new approach to cancer therapy (14). A number of stimulators and inhibitors regulate angiogenesis (15). In the case of PKD1, a consensus exists with regard to its proangiogenic and thus proproliferative role whatever the cell model [endothelial progenitor cells (EPC) or cell lines] or the species (human or even zebrafish).…”

Section: Pkd1 Stimulates Angiogenesis a Key Determinant In Cancer Dementioning

confidence: 99%

Deciphering the Role of Protein Kinase D1 (PKD1) in Cellular Proliferation

Youssef

Ricort

2019

Molecular Cancer Research

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Protein kinase D1 (PKD1) is a serine/threonine kinase that belongs to the calcium/calmodulin-dependent kinase family, and is involved in multiple mechanisms implicated in tumor progression such as cell motility, invasion, proliferation, protein transport, and apoptosis. While it is expressed in most tissues in the normal state, PKD1 expression may increase or decrease during tumorigenesis, and its role in proliferation is context-dependent and poorly understood. In this review, we present and discuss the current landscape of studies investigating the role of PKD1 in the proliferation of both cancerous and normal cells. Indeed, as a potential therapeutic target, deciphering whether PKD1 exerts a pro-or antiproliferative effect, and under what conditions, is of paramount importance.

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Dose dependent effects of cadmium on tumor angiogenesis

Cited by 41 publications

References 136 publications

Chronic long‐term exposure to cadmium air pollution and breast cancer risk in the French E3N cohort

Chronic long‐term exposure to cadmium air pollution and breast cancer risk in the French E3N cohort

Cadmium Induces Glomerular Endothelial Cell–Specific Expression of Complement Factor H via the −1635 AP-1 Binding Site

Deciphering the Role of Protein Kinase D1 (PKD1) in Cellular Proliferation

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