scholarly journals Increased expression of both insulin receptor substrates 1 and 2 confers increased sensitivity to IGF-1 stimulated cell migration

2009 ◽  
Vol 16 (2) ◽  
pp. 635-647 ◽  
Author(s):  
Gail E de Blaquière ◽  
Felicity E B May ◽  
Bruce R Westley
Keyword(s):  
Breast Cancer ◽  
Cell Migration ◽  
Insulin Receptor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Type I ◽  
Migratory Response ◽  
Type I Igf Receptor ◽  
Igf Receptor ◽  
Mcf 7

Insulin-like growth factors (IGFs) are thought to promote tumour progression and metastasis in part by stimulating cell migration. Insulin receptor substrate-1 (IRS-1) and IRS-2 are multisite docking proteins positioned immediately downstream from the type I IGF and insulin receptors. IRS-2 but not IRS-1 has been reported to be involved in the migratory response of breast cancer cells to IGFs. The purpose of this investigation was to determine if IRS-1 is involved in, and to assess the contributions of IRS-1 and IRS-2 to, the migratory response of breast cancer cells to IGFs. The expression of IRS-1 and IRS-2 varied considerably between ten breast cancer cell lines. Oestrogen increases expression of the type I IGF receptor, IRS-1 and IRS-2 in MCF-7 and ZR-75 cells. Oestrogens may control the sensitivity of breast cancer cells to IGFs by regulating the expression of components of the IGF signal transduction pathway. The migratory response to a range of IGF-1 concentrations was measured in MCF-7 and MDA-MB-231 breast cancer cells in which IRS-1 and IRS-2 levels were modulated using a doxycycline-inducible expression system. Induction of both IRS-1 and IRS-2 expression increased the sensitivity of the migratory response to IGF-1 but did not increase the magnitude of the response stimulated at higher concentrations of IGF-1. Knockdown of IRS-1, IRS-2 and the type I IGF receptor in MCF-7 and MDA-MB-2231 cells decreased sensitivity to IGF-1. We conclude that both IRS-1 and IRS-2 control the migratory response of breast cancer cells to IGF-1 and may, therefore, be key molecules in determining breast cancer spread.

Detection and downregulation of type I IGF receptor expression by antibody-conjugated quantum dots in breast cancer cells

2008 ◽  
Vol 114 (2) ◽  
pp. 277-285 ◽  
Author(s):  
Hua Zhang ◽  
Deepali Sachdev ◽  
Chun Wang ◽  
Allison Hubel ◽  
Martine Gaillard-Kelly ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Quantum Dots ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Receptor Expression ◽  
Type I ◽  
Type I Igf Receptor ◽  
Igf Receptor

Type I IGF receptor and acquired tamoxifen resistance in oestrogen-responsive human breast cancer cells

1993 ◽  
Vol 29 (16) ◽  
pp. 2256-2264 ◽  
Author(s):  
Lynda R. Wiseman ◽  
Michael D. Johnson ◽  
Alan E. Wakeling ◽  
Anne E. Lykkesfeldt ◽  
Felicity E.B. May ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Tamoxifen Resistance ◽  
Type I ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Type I Igf Receptor ◽  
Igf Receptor

The Effect of Acetylsalicylic Acid (ASA) on the Mechanical Properties of Breast Cancer Epithelial Cells

2022 ◽  
Vol 17 ◽  
Author(s):  
Dornaz Milani ◽  
Siamak Khoramymehr ◽  
Behrouz Vasaghi-Gharamaleki
Keyword(s):  
Breast Cancer ◽  
Mechanical Properties ◽  
Cell Migration ◽  
Cancer Cells ◽  
Young’S Modulus ◽  
Actin Filaments ◽  
Breast Cancer Cells ◽  
Young's Modulus ◽  
Mcf 7 ◽  
Cell Strength

Background: In most communities, the risk of developing breast cancer is increasing. By affecting the cyclooxygenase 1 and 2 (COX-1 and COX-2) enzymes and actin filaments, acetylsalicylic acid (Aspirin) has been shown to reduce the risk of breast cancer and prevent cell migration in both laboratory and clinical studies. Methods: The purpose of this study is to determine the mechanical properties of normal and cancerous breast tissue cells, as well as the short-term effect of aspirin on cancer cells. To this end, the mechanical properties and deformation of three cell types were investigated: healthy MCF-10 breast cells, MCF-7 breast cancer cells, and MCF-7 breast cancer cells treated with a 5 µM aspirin solution. Atomic Force Microscopy (AFM) was used to determine the mechanical properties of the cells. Cell deformation was analyzed in all groups, and Young's modulus was calculated using the Hertz model. Result: According to the obtained data, cancer cells deformed at a rate half that of healthy cells. Nonetheless, when aspirin was used, cancer cells deformed similarly to healthy cells. Additionally, healthy cells' Young's modulus was calculated to be approximately three times that of cancer cells, which was placed closer to that of healthy cells by adding aspirin to Young's modulus. Conclusion: Cell strength appears to have increased due to aspirin's intervention on actin filaments and cytoskeletons, and the mechanical properties of breast cancer cells have become more similar to those of normal cells. The likelihood of cell migration and metastasis decreases as cell strength increases.

On-chip cell migration assay for quantifying the effect of ethanol on MCF-7 human breast cancer cells

2011 ◽  
Vol 10 (6) ◽  
pp. 1333-1341 ◽  
Author(s):  
Xiaowen Huang ◽  
Li Li ◽  
Qin Tu ◽  
Jianchun Wang ◽  
Wenming Liu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Migration Assay ◽  
On Chip ◽  
Mcf 7

scholarly journals Proton pump inhibitors enhance chemosensitivity, promote apoptosis, and suppress migration of breast cancer cells

2020 ◽  
Vol 70 (2) ◽  
pp. 179-190 ◽  
Author(s):  
Worood G. Ihraiz ◽  
Mamoun Ahram ◽  
Sanaa K. Bardaweel
Keyword(s):  
Breast Cancer ◽  
Cell Migration ◽  
Synergistic Effect ◽  
Cancer Cells ◽  
Cell Lines ◽  
Proton Pump ◽  
Breast Cancer Cells ◽  
Combined Treatment ◽  
Combined Effects ◽  
Mcf 7

AbstractBreast cancer is the most common cancer and is the leading cause of cancer deaths among women worldwide. Despite the availability of numerous therapeutics for breast cancer management, cytotoxicity and emergence of drug resistance are major challenges that limit their benefits. The acidic microenvironment surrounding tumor cells is a common feature inducing cancer cell invasiveness and chemoresistance. Proton pump inhibitors (PPIs) are one of the most commonly prescribed drugs for the treatment of acid-related conditions. PPIs have been reported to exhibit antitumorigenic effects in many cancer types. In this study, the anti-proliferative and anti-migratory effects of PPIs in three breast cancer cell lines; MCF-7, T47D, and MDA-MB-231 cells, have been investigated. In addition, the combined effects of PPIs with anticancer drugs, as well as the mechanism of PPI-mediated anti-proliferative activity were evaluated. The anti-proliferative and combined effects of PPIs were evaluated by MTT assay. Cell migration was assessed using the wound-healing assay. The mechanism of cell death was assessed using annexin V-FITC/propidium iodide staining flow cytometry method. Our results indicated that PPIs treatment significantly inhibited the growth of breast cancer cells in a dose-dependent manner. The antiproliferative activity of PPIs was significantly induced by apoptosis in all tested cell lines. The combined treatment of PPIs with doxorubicin resulted in a synergistic effect in all cell lines, whereas the combined treatment with raloxifene exhibited synergistic effect in T47D cells only and additive effects in MDA-MB-231 and MCF-7 cells. In addition, PPIs treatment significantly reduced cell migration in MDA-MB-231 cells. In conclusion, the addition of PPIs to the treatment regimen of breast cancer appears to be a promising strategy to potentiate the efficacy of chemotherapy and may suppress cancer metastasis.

RNAi-mediated silencing of insulin receptor substrate 1 (IRS-1) enhances tamoxifen-induced cell death in MCF-7 breast cancer cells

2006 ◽  
Vol 98 (2) ◽  
pp. 440-450 ◽  
Author(s):  
Gregory Cesarone ◽  
Cecilia Garofalo ◽  
Marc T. Abrams ◽  
Olga Igoucheva ◽  
Vitali Alexeev ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Insulin Receptor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Insulin Receptor Substrate ◽  
Insulin Receptor Substrate 1 ◽  
Mcf 7
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