Consumption of high-fat diet induces tumor progression and epithelial–mesenchymal transition of colorectal cancer in a mouse xenograft model

Tang, Feng; Pai, Man Hui; Chiang, En‐Pei Isabel

doi:10.1016/j.jnutbio.2011.07.011

Cited by 69 publications

(45 citation statements)

References 52 publications

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“…High red meat consumption is a significant CRC risk factor (WCRF, 2007;Hu et al, 2013), as evidenced by the promotive effect of high red meat consumption on CRC risk in this study. One mechanism for the link between high-red meat diets and CRC is attributed to high fat levels (Tang et al, 2012). Animal fats, particularly from red meat, are a risk factor for colon cancer among women (Macrae, 1993).…”

Section: Discussionmentioning

confidence: 99%

“…Smoked meat significantly influences the promotion of colon carcinogenesis (Santarelli et al, 2010). During the preparation of smoked meat, N-nitroso compounds are formed in the meat as it is pickled with salt, and heterocyclic amines are also formed as the meat is cooked at high temperature; both compounds are strong carcinogens for CRC (Bingham, 1999;Knize et al, 1999;Tang et al, 2012). SNP43 is associated with intraabdominal fat, a large waist circumference, and increased serum cholesterol, all of which can be caused by high consumption of red and smoked meat.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Calpain-10 SNP43 and SNP19 Polymorphisms and Colorectal Cancer: a Matched Case-control Study

Yuan²,

Luan³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Objective: Insulin resistance (IR) is an established risk factor for colorectal cancer (CRC). Given that CRC and IR physiologically overlap and the calpain-10 gene (CAPN10) is a candidate for IR, we explored the association between CAPN10 and CRC risk. Methods: Blood samples of 400 case-control pairs were genotyped, and the lifestyle and dietary habits of these pairs were recorded and collected. Unconditional logistic regression (LR) was used to assess the effects of CAPN10 SNP43 and SNP19, and environmental factors. Both generalized multifactor dimensionality reduction (GMDR) and the classification and regression tree (CART) were used to test gene-environment interactions for CRC risk. Results: The GA+AA genotype of SNP43 and the Del/Ins+Ins/Ins genotype of SNP19 were marginally related to CRC risk (GA+AA: OR = 1.35, 95% CI = 0.92-1.99; Del/Ins+Ins/ Ins: OR = 1.31, 95% CI = 0.84-2.04). Notably, a high-order interaction was consistently identified by GMDR and CART analyses. In GMDR, the four-factor interaction model of SNP43, SNP19, red meat consumption, and smoked meat consumption was the best model, with a maximum cross-validation consistency of 10/10 and testing balance accuracy of 0.61 (P < 0.01). In LR, subjects with high red and smoked meat consumption and two risk genotypes had a 6.17-fold CRC risk (95% CI = 2.44-15.6) relative to that of subjects with low red and smoked meat consumption and null risk genotypes. In CART, individuals with high smoked and red meat consumption, SNP19 Del/Ins+Ins/Ins, and SNP43 GA+AA had higher CRC risk (OR = 4.56, 95%CI = 1.94-10.75) than those with low smoked and red meat consumption. Conclusions: Though the single loci of CAPN10 SNP43 and SNP19 are not enough to significantly increase the CRC susceptibility, the combination of SNP43, SNP19, red meat consumption, and smoked meat consumption is associated with elevated risk.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Calpain-10 SNP43 and SNP19 Polymorphisms and Colorectal Cancer: a Matched Case-control Study

Yuan²,

Luan³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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“…Is it a consequence of obesity or do the causes of obesity independently promote the carcinogenic process? In response to this intriguing question, it is interesting to note that multiple models have now been reported wherein transplanted and/or spontaneous tumors, including breast cancer, are promoted by high-fat diet in the absence of obesity (26)(27)(28)(29)(30).…”

Section: Articles By Iyengar Et Al Published In This Issue Cancer Prmentioning

confidence: 99%

Crown-like Structures in Breast Adipose Tissue from Normal Weight Women: Important Impact

Berger

2017

Cancer Prevention Research

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Crown-like structures (CLS), composed of macrophages surrounding dead or dying adipocytes, are a histologic hallmark of the proinflammatory process by which adipose tissue contributes to the increased risk and worse prognosis of breast cancer in obese, postmenopausal patients. In this issue of Cancer Prevention Research, Iyengar and colleagues report the intriguing finding that CLS can be identified in a significant proportion of normal-BMI women undergoing mastectomy for breast cancer risk reduction or therapy. This surprising observation suggests that some normal weight women may have similar mechanisms driving initiation and/or progression of breast cancer as those contributing to the increased incidence and worse prognosis of breast cancer in obese postmenopausal women. The possibility of a common mechanism in both lean and obese women provides added impetus to more fully define this process and evaluate its important implications for prevention and screening strategies as well as therapeutic interventions. Cancer Prev Res; 10(4); 223-5. Ó2017AACR.

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“…It has been found that NF-kB suppresses the expression of epithelial specific genes, E-cadherin and desmoplakin, and induces the expression of the mesenchymal specific gene vimentin (Tang et al, 2012). Repression of E-cadherin expression by the transcription factor Snail is a central event during the loss of epithelial phenotype.…”

Section: N F -K B a C T I V A T I O N A N D E P I T H E L I A Lmesencmentioning

confidence: 99%

Epithelial-mesenchymal Transition and Its Role in the Pathogenesis of Colorectal Cancer

Zhu¹,

Gao²,

Wu³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Epithelial-to-mesenchymal transition (EMT) is a collection of events that allows the conversion of adherent epithelial cells, tightly bound to each other within an organized tissue, into independent fibroblastic cells possessing migratory properties and the ability to invade the extracellular matrix. EMT contributes to the complex architecture of the embryo by permitting the progression of embryogenesis from a simple single-cell layer epithelium to a complex three-dimensional organism composed of both epithelial and mesenchymal cells. However, in most tissues EMT is a developmentally restricted process and fully differentiated epithelia typically maintain their epithelial phenotype. Recently, elements of EMT, specially the loss of epithelial markers and the gain of mesenchymal markers, have been observed in pathological states, including epithelial cancers. Increasing evidence has confirmed its presence in human colon during colorectal carcinogenesis. In general, chronic inflammation is considered to be one of the causes of many human cancers including colorectal cancer(CRC). Accordingly, epidemiologic and clinical studies indicate that patients affected by ulcerative colitis and Crohn's disease, the two major forms of inflammatory bowel disease, have an increased risk of developing CRC. A large body of evidence supports roles for the SMAD/STAT3 signaling pathway, the NF-kB pathway, the Ras-mitogenactivated protein kinase/Snail/Slug and microRNAs in the development of colorectal cancers via epithelial-tomesenchymal transition. Thus, EMT appears to be closely involved in the pathogenesis of colorectal cancer, and analysis refered to it can yield novel targets for therapy.

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Consumption of high-fat diet induces tumor progression and epithelial–mesenchymal transition of colorectal cancer in a mouse xenograft model

Cited by 69 publications

References 52 publications

Calpain-10 SNP43 and SNP19 Polymorphisms and Colorectal Cancer: a Matched Case-control Study

Calpain-10 SNP43 and SNP19 Polymorphisms and Colorectal Cancer: a Matched Case-control Study

Crown-like Structures in Breast Adipose Tissue from Normal Weight Women: Important Impact

Epithelial-mesenchymal Transition and Its Role in the Pathogenesis of Colorectal Cancer

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