Dietary animal-derived iron and fat intake and breast cancer risk in the Shanghai Breast Cancer Study

Kallianpur, Asha R.; Lee, Sang Ah; Gao, Yu Tang; Lü, Wei; Ying, Zheng; Ruan, Zhi; Dai, Qi; Gu, Kai; Shu, Xiao Ou; Wang, Zheng

doi:10.1007/s10549-007-9538-3

Cited by 58 publications

(64 citation statements)

References 42 publications

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“…To date, dietary intake of iron is assumed to be an important source for elevated iron store. For example, a case-control survey of 3452 breast cancer patients and 3474 age-frequency-matched healthy controls in China showed that intake of meat-derived hemeiron increased the risk of breast cancer in Chinese women [32]. Similar observations were found for cancer patients in the US [33].…”

Section: Iron and Il-6 Jointly Promoted Tumor Cell Growthmentioning

confidence: 62%

Disordered hepcidin–ferroportin signaling promotes breast cancer growth

Zhang

Chen

Guo

et al. 2014

Cellular Signalling

111

136

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Iron homeostasis is strictly governed in mammals; however, disordered iron metabolism (such as excess iron burden) is recognized as a risk factor for various types of diseases including cancers. Burgeoning evidence indicates that the central signaling of iron homeostasis, the hepcidin-ferroportin axis, is misregulated in cancers. Nonetheless, the mechanisms of misregulated expression of iron-related genes along this signaling in cancers remain largely unknown. In the current study, we found increased levels of serum hepcidin in breast cancer patients. Reduction of hepatic hepcidin through administration of heparin restrained tumorigenic properties of breast tumor cells. Mechanistic investigation revealed that increased iron, bone morphogenetic protein-6 (BMP6) and interleukin-6 (IL-6) jointly promoted the synthesis of hepatic hepcidin. Tumor hepcidin expression was marginally increased in breast tumors relative to adjacent tissues. In contrast, tumor ferroportin concentration was greatly reduced in breast tumors, especially in malignant tumors, compared to adjacent tissues. Elevation of ferroportin concentration inhibited cell proliferation in vitro and in vivo by knocking down tumor hepcidin expression. Additionally, increased IL-6 was demonstrated to jointly enhance the tumorigenic effects of iron through enforcing cell growth. Our combined data overall deciphered the machinery that altered the hepcidin-ferroportin signaling in breast cancers. Thus, targeting the hepcidin-ferroportin signaling would represent a promising therapeutics to restrain breast cancer growth.

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Section: Iron and Il-6 Jointly Promoted Tumor Cell Growthmentioning

confidence: 62%

Disordered hepcidin–ferroportin signaling promotes breast cancer growth

Zhang

Chen

Guo

et al. 2014

Cellular Signalling

111

136

View full text Add to dashboard Cite

show abstract

“…A large number of studies have delineated the considerable contribution altered iron metabolism to tumor development (Bystrom et al, 2012;Richardson et al, 2009;Torti and Torti, 2011). For example, case-control surveys of breast cancer patients revealed that intake of meat-derived heme-iron increased the risk of breast cancer (Ferrucci et al, 2009;Kallianpur et al, 2008). Therefore, our current study provides an additional novel mechanism by which PCBs instigate cancer progression through disturbing systemic iron homeostasis.…”

Section: Resultsmentioning

confidence: 81%

PCB-77 disturbs iron homeostasis through regulating hepcidin gene expression

Wang

Zhang

Lin

et al. 2013

Gene

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a b s t r a c t a r t i c l e i n f oPCBs are a family of persistent environmental toxicants with a wide spectrum of toxic features, such as immunotoxicity, hepatoxicity, endocrine disruption effects, and oncogenic effects. To date, little has been done to investigate the potential influence of PCB exposure on iron metabolism. Deregulated iron would lead to either iron deficiency or iron excess, coupled with various diseases such as anemia or hemochromatosis. Iron metabolism is strictly governed by the hepcidin-ferroportin axis, and hepcidin is the key regulator that is secreted by hepatocytes. Here, we found that PCB-77 could go through plasma membrane and accumulate in hepatocytes. PCB-77 was demonstrated to suppress hepcidin expression in HepG2 and L-02 hepatocytes. Moreover, hepatic hepcidin was observed to be inhibited in mice upon administration of PCB-77. Due to reduced hepcidin concentration, serum iron content was increased, with a significant reduction of splenic iron content. Together, we deciphered the molecular mechanism responsible for PCB-conducted disturbance on iron homeostasis, i.e. through misregulating hepatic hepcidin expression.

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“…Articles accepted for analysis (n = 33) DOI:http://dx.doi.org/10.7314/APJCP.2014.15.3.1291 Association between Dietary Factors andBreast Cancer Risk among Chinese Females: Meta-analysis Li et al, 2006;Shen et al, 2006;Zhu et al, 2006;Wang, 2007;Kallianpur et al, 2008;Ren, 2008;Rong et al, 2008;Wang et al, 2008;Fang et al, 2009;Zhang et al, 2009;Zhou et al, 2009;Cheng et al, 2010;Guo et al, 2010;Zheng et al, 2010;Wang et al, 2011;Liang, 2012;Yao et al, 2012;Yu et al, 2012;Zhang et al, 2012;Bo et al, 2013;Luo et al, 2013). Four duplicate publications were excluded (Wang, 2000;Zhang et al, 2003;Zou et al, 2003;Fang et al, 2009).…”

Section: Resultsmentioning

confidence: 99%