IGF-I Receptor-induced Cell-Cell Adhesion of MCF-7 Breast Cancer Cells Requires the Expression of Junction Protein ZO-1

Mauro, Loredana; Bartucci, Monica; Morelli, Catia; Andò, Sebastiano; Surmacz, Eva

doi:10.1074/jbc.m106673200

Cited by 58 publications

(58 citation statements)

References 25 publications

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“…Specifically, we demonstrated that IGF-I treatment, overexpression of IGF-IR and overexpression of IGF-I, all resulted in increased cell-cell adhesion (Bracke et al, 1993;Deman et al, 1995;Vermeulen et al, 1995;Guvakova and Surmacz, 1997;Surmacz et al, 1998;Mauro et al, 2001). Importantly, the effects of IGF-IR overexpression and IGF-I treatment on cell-cell adhesion were blocked with anti-E-cad antibody and were absent in E-cad-negative MDA-MB-231 breast cancer cells (Guvakova and Surmacz, 1997;Mauro et al, 2001).…”

Section: Igf-ir Modulates the E-cadherin Complexmentioning

confidence: 80%

“…For instance, re-expression of Ecad in E-cad-negative mammary breast cancer cells induced cell-cell adhesion and reduced bone and lung metastasis (Takeichi, 1990;Frixen et al, 1991;Mareel et al, 1994;Mbalaviele et al, 1996;Meiners et al, 1998;Mauro et al, 2001). Similarly, the transgenic E-cad expression in nude mice blocked metastatic process, while the expression of a dominant negative E-cad promoted early invasion and metastasis in a pancreatic beta-cell carcinogenesis model (Perl et al, 1998).…”

Section: Cell-cell Adhesion and The E-cadherin Complexmentioning

confidence: 99%

“…1A) (Guvakova and Surmacz, 1997;Surmacz et al, 1998;Mauro et al, 2001). The studies on molecular mechanisms of IGF-IR-dependent cell-cell adhesion indicated that IGF-IR overexpression or IGF-I treatment of MCF-7 cells did not alter the expression or tyrosine phosphorylation of E-cad or alpha-, beta-, or gamma-catenins (Guvakova and Surmacz, 1997;Surmacz et al, 1998;Mauro et al, 2001). Instead, IGF-I-increased cell-cell adhesion coincided with overexpression of zonula occludens protein-1 (ZO-1).…”

Section: Igf-ir Modulates the E-cadherin Complexmentioning

confidence: 99%

“…Different elements of IGF-IR signaling system (IGF-IR, IRS-1, SHC) also interact with the molecules involved in the regulation of cell-cell adhesion, and IGF-I-dependent cell-cell adhesion has been shown to improve cell survival (Guvakova and Surmacz, 1997;Mareel et al, 1997;Surmacz et al, 1998;Surmacz, 2000;Valentinis et al, 1998;Mauro et al, 2001).…”

mentioning

confidence: 99%

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Role of the IGF‐I receptor in the regulation of cell–cell adhesion: Implications in cancer development and progression

Mauro

Salerno

Morelli

et al. 2002

Journal Cellular Physiology

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The insulin-like growth factor-I receptor (IGF-IR) is a ubiquitous multifunctional tyrosine kinase that has an important role in normal cell growth and development. However, abnormal stimulation of IGF-IR signaling has been implicated in the development of different types of tumors. The strong antiapoptotic activity of IGF-IR has been recognized as critical in IGF-I-dependent tumorigenesis, however, the impact of other IGF-IR functions, such as regulation of cell-cell and cell-matrix adhesion are also increasingly acknowledged. Here, on the model of breast cancer cells, we discuss how IGF-IR-dependent regulation of intercellular adhesion may affect cell survival, resistance to antiestrogens, and invasion.

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Section: Igf-ir Modulates the E-cadherin Complexmentioning

confidence: 80%

Section: Cell-cell Adhesion and The E-cadherin Complexmentioning

confidence: 99%

Section: Igf-ir Modulates the E-cadherin Complexmentioning

confidence: 99%

mentioning

confidence: 99%

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Role of the IGF‐I receptor in the regulation of cell–cell adhesion: Implications in cancer development and progression

Mauro

Salerno

Morelli

et al. 2002

Journal Cellular Physiology

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“…It was recently reported that, in breast cancer cells, IGF-I induces the phosphorylation of ZO-1, a scaffolding protein that resides in the tight junctions. 50 In the vasculature, hyperphosphorylation of ZO-1 usually coincides with its departure from the tight junctions into the cytoplasm and with increased vascular permeability. 51 In addition, IGF-I may also lead to increased permeability via the up-regulation of VEGF.…”

Section: Discussionmentioning

confidence: 99%

Insulin-Like Growth Factor-I Plays a Pathogenetic Role in Diabetic Retinopathy

Poulaki

Joussen

Mitsiades

et al. 2004

The American Journal of Pathology

138

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Although the molecular pathophysiology of diabetic retinopathy, the current leading cause of blindness in Western societies, 1 is not fully elucidated, studies have documented a pivotal role for leukocyte adherence within the retinal vasculature. The adhesion of leukocytes to the retinal endothelium is a process that depends on ␤ 2 integrin-intercellular adhesion molecule (ICAM)-1 interactions and leads to breakdown of the blood-retinal barrier. 2 These data, in combination with our previous findings that aggressive anti-inflammatory therapy suppressed leukocyte adhesion and blood retinal breakdown in a relevant animal model, 3 support the hypothesis that a chronic subclinical inflammation may underlie much of the vascular pathology of diabetic retinopathy. 4 These vascular pathological findings are orchestrated by vascular endothelial growth factor (VEGF), a factor that potently promotes the growth and maintenance of endothelial cells and the formation of new vessels, and is implicated in both background and proliferative diabetic retinopathy. 5-11 Intraocular VEGF levels are increased in diabetic patients with blood-retinal barrier breakdown and neovascularization, 5,10,12,13 whereas the specific inhibition of VEGF prevents these complications in animal models. 7,11,14 Therefore, regulation of VEGF expression could conceivably be both a mediator for converging local and systemic stimuli modulating vessel pathophysiology, as well as a target for therapeutic intervention. Within a constellation of known modulators of VEGF expression that can possibly function at the transcriptional [through AP-1, AP-2, steroid hormone receptors, p53, and nuclear factor (NF-B)] or posttranscriptional level, [15][16][17][18] hypoxia is the most potent inducer of VEGF transcription in vivo; its effects are mainly mediated by the helix-loop helix (bHLH)-PAS transcription factor HIF-1␣, which heterodimerizes with the bHLH-PAS protein ARNT or HIF-1␤, 19 -22 and binds to consensus and ancillary hypoxia-response elements (HREs) in the VEGF promoter. 21,[23][24][25]

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Expression of insulin‐like growth factor‐1 receptor in circulating tumor cells of patients with breast cancer is associated with patient outcomes

et al. 2017

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In patients with breast cancer, markers of aggressiveness such as dysregulation of the insulin‐like growth factor receptor (IGF1R) system and E‐cadherin loss are commonly observed. Reduced IGF1R expression is correlated with decreased E‐cadherin levels and increased cell motility. We assessed IGF1R and E‐cadherin expression in circulating tumor cells (CTCs) in patients with breast cancer. Peripheral blood mononuclear cells of early (n = 87)‐ and metastatic (n = 126)‐stage breast cancer patients (obtained prior to adjuvant and first‐line chemotherapy) were evaluated using double immunofluorescence (IF) staining for cytokeratin (CK) and IGF1R. Triple IF using CK, IGF1R, and E‐cadherin antibodies was performed in selected CTC(+) patients. IGF1R(+) CTCs were more frequently observed in early disease than in metastatic disease (86% vs 68% of CTCs, P = 0.04) stage, whereas IGF1R(−) CTCs were more common in metastatic than in early disease (32% vs 14% of CTCs, P = 0.002). 100% of CTC(+) patients with early disease, compared to 79% of those with metastatic disease, harbored IGF1R(+) CTCs (P = 0.007). Patients with early disease and exclusively IGF1R(+) CTCs had longer disease‐free (P = 0.02) and overall survival (P = 0.001) compared to patients with both IGF1R(+) and IGF1R(−) CTC populations. 67% of early‐stage CTC(+) patients evaluated had exclusively IGF1R(+)/E‐cadherin(+) CTCs, 33% also had IGF1R(−)/E‐cadherin(−) CTCs, and none had exclusively IGF1R(−)/E‐cadherin(−) CTCs compared to 17%, 75%, and 8% of metastatic patients, respectively (P = 0.027). Similarly, in paired samples of patients with early disease that progressed to metastatic disease, the proportion of IGF1R(+)/E‐cadherin(+) CTCs was reduced and IGF1R(−)/E‐cadherin(−) CTCs were increased in the metastatic stage compared to early disease stage. IGF1R(+) CTCs are commonly detected in breast cancer, and their frequency decreases in the metastatic disease stage. IGF1R(+)/E‐cadherin(+) CTCs also decrease in metastatic patients. IGF1R(+) CTCs are associated with favorable outcomes in early disease stage, suggesting that IGF1R expression is correlated with reduced metastatic potential in breast cancer.

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IGF-I Receptor-induced Cell-Cell Adhesion of MCF-7 Breast Cancer Cells Requires the Expression of Junction Protein ZO-1

Cited by 58 publications

References 25 publications

Role of the IGF‐I receptor in the regulation of cell–cell adhesion: Implications in cancer development and progression

Role of the IGF‐I receptor in the regulation of cell–cell adhesion: Implications in cancer development and progression

Insulin-Like Growth Factor-I Plays a Pathogenetic Role in Diabetic Retinopathy

Expression of insulin‐like growth factor‐1 receptor in circulating tumor cells of patients with breast cancer is associated with patient outcomes

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