Insulin-like growth factors in human breast cancer

Ellis, Matthew J.; Jenkins, Sara; Hanfelt, John; Redington, Maura E.; Taylor, Marian; Leek, Russel; Siddle, Ken; Harris, Adrian L.

doi:10.1007/978-1-4615-5195-9_21

Cited by 73 publications

(31 citation statements)

References 41 publications

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“…Most in vitro studies have shown that cancer cells modulated by EGFR activation have increased propensity for mitosis, proapoptosis, chemoresistance and angiogenesis. 4,5,[13][14][15][16]23 In addition, some reports have indicated that membranous EGFR activation is responsible for the regulation of intercellular adhesion such as cell-cell and cellmatrix adhesion. IGF1R activation has also been …”

Section: Discussionmentioning

confidence: 99%

“…[1][2][3][4][5][6] In addition, the ligand-binding activation of IGF1R through the PI3K signaling pathway is known to promote proliferation in some cancer cell lines, and to protect many different cell types from a variety of proapoptotic damage. 3,4,7,[8][9][10] Among the tyrosine kinase receptor families, the mechanism of action of the epidermal growth factor receptor (EGFR) family, especially EGFR and HER-2 (c-erbB2), is that which has been best characterized. 11,12 EGFR and HER-2 are also thought to be involved in the development of cancers.…”

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confidence: 99%

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Potential crosstalk between insulin-like growth factor receptor type 1 and epidermal growth factor receptor in progression and metastasis of pancreatic cancer

et al. 2006

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The insulin-like growth factor receptor type 1 (IGF1R) and epidermal growth factor receptor (EGFR) are reportedly overexpressed in pancreatic cancer. However, the correlation between activated EGFR and IGF1R and their clinicopathological implications still remain unclear. The cellular localization and overexpression of IGF1R and EGFR were investigated immunohistochemically in primary invasive ductal pancreatic carcinomas obtained from 74 patients who underwent radical surgical resection. We also compared the status of IGF1R and EGFR overexpression between primary tumors and hepatic metastatic tumors obtained from 44 autopsied patients. Among the 74 surgically resected primary tumors, cytoplasm-and membrane-dominant EGFR overexpression was detected in 22 (30%) and 7 (9%), respectively, whereas cytoplasm-and membranedominant IGF1R overexpression was detected in 8 (11%) and 28 (38%), respectively. Membrane-dominant EGFR and cytoplasm-dominant IGF1R were more frequent in lower-grade tumors and correlated with favorable prognosis, whereas cytoplasm-dominant EGFR and membrane-dominant IGF1R were more frequent in highergrade tumors and correlated with poor prognosis. In 36 autopsy specimens of pancreatic tumor with concurrent overexpression of IGF1R and EGFR, there was an inverse correlation between the IGF1R and EGFR localization patterns (P ¼ 0.001). In the hepatic metastatic tumors obtained by autopsy, the incidences of both IGF1R and EGFR overexpression were much higher than in the surgically resected primary tumors. More than half of the autopsy cases consistently showed membrane-dominant EGFR expression in both the primary tumor and hepatic metastases, whereas IGF1R expression showed considerable variation. Crosstalk between differently localized IGF1R and EGFR might play a role in determining the biological aggressiveness of pancreatic cancer, although their cellular localization may often alter during the process of metastasis.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Potential crosstalk between insulin-like growth factor receptor type 1 and epidermal growth factor receptor in progression and metastasis of pancreatic cancer

et al. 2006

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“…48 Finally, insulin and IGF-I that are known to be important for breast cancer cell growth, were also removed from FBS by dextran-charcoal. 46,49 In conclusion, we have successfully developed a novel human breast cancer cell model in which the expression of c-myc can be stringently and rapidly regulated. This cell model has allowed the demonstration that c-myc expression alone is sufficient to significantly reverse the growth inhibitory effects of the pure estrogen antagonist ICI 182,780.…”

Section: Discussionmentioning

confidence: 99%

C‐myc gene expression alone is sufficient to confer resistance to antiestrogen in human breast cancer cells

Venditti

Iwasiow

Orr

et al. 2002

Intl Journal of Cancer

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“…The insulin-like growth factor system (IGF), which comprises a complex network of ligands (IGF-I and IGF-II), cognate receptors (type I, type II IGF receptors, and insulin receptor), IGF-binding proteins, and IGF-binding protein proteases, plays multiple roles in normal mammary gland and breast cancer (6)(7)(8)(9)(10). With the studies of cytokines, some proteins are found to collaborate with special cytokines in cancer cells.…”

Section: Introductionmentioning

confidence: 99%

Enhanced Expression of Rab27A Gene by Breast Cancer Cells Promoting Invasiveness and the Metastasis Potential by Secretion of Insulin-Like Growth Factor-II

Wang

Zhang

et al. 2008

Molecular Cancer Research

102

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In addition to the functions of transporting melanosome in melanocytes and releasing contents of lytic granules in CTLs, Rab27A was recently shown to be involved in exocytosis of insulin and chromaffin granules in endocrine cells; it was also reported to be expressed in an exceptionally broad range of specialized secretory cells. As autocrine and paracrine cytokines are essential for invasion and metastasis in some solid tumors, blocking them may be an effective strategy to prevent tumor dissemination. In the present study, we show that Rab27A is associated with invasive and metastatic potentials of human breast cancer cells. The overexpression of Rab27A protein redistributed the cell cycle and increased the invasive and metastatic abilities in breast cancer cells both in vitro and in vivo. We also certified that Rab27A conferred the invasive and metastatic phenotypes on breast cancer cells by promoting the secretion of insulin-like growth factor-II (IGF-II), which regulates the expression of p16, vascular endothelial growth factor, matrix metalloproteinase-9, cathepsin D, cyclin D1, and urokinase-type plasminogen activator. These data provide functional evidence that Rab27A acts as a novel mediator of invasion and metastasis promotion in human breast cancer cells, at least in part, through regulating the secretion of IGF-II, suggesting that synergistic suppression of Rab27A and IGF-II activities holds a promise for preventing breast cancer invasion and metastasis.

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Insulin-like growth factors in human breast cancer

Cited by 73 publications

References 41 publications

Potential crosstalk between insulin-like growth factor receptor type 1 and epidermal growth factor receptor in progression and metastasis of pancreatic cancer

Potential crosstalk between insulin-like growth factor receptor type 1 and epidermal growth factor receptor in progression and metastasis of pancreatic cancer

C‐myc gene expression alone is sufficient to confer resistance to antiestrogen in human breast cancer cells

Enhanced Expression of Rab27A Gene by Breast Cancer Cells Promoting Invasiveness and the Metastasis Potential by Secretion of Insulin-Like Growth Factor-II

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