scholarly journals Biomechanical and Biophysical Properties of Breast Cancer Cells Under Varying Glycemic Regimens

2020 ◽  
Vol 14 ◽  
pp. 117822342097236
Author(s):  
Diganta Dutta ◽  
Xavier-Lewis Palmer ◽  
Jose Ortega-Rodas ◽  
Vasundhara Balraj ◽  
Indrani Ghosh Dastider ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Young’S Modulus ◽  
High Glucose ◽  
Breast Cancer Cells ◽  
Mammary Epithelial Cells ◽  
Young's Modulus ◽  
Malignant Cells ◽  
Biophysical Properties ◽  
Mcf 7

Diabetes accelerates cancer cell proliferation and metastasis, particularly for cancers of the pancreas, liver, breast, colon, and skin. While pathways linking the 2 disease conditions have been explored extensively, there is a lack of information on whether there could be cytoarchitectural changes induced by glucose which predispose cancer cells to aggressive phenotypes. It was thus hypothesized that exposure to diabetes/high glucose alters the biomechanical and biophysical properties of cancer cells more than the normal cells, which aids in advancing the cancer. For this study, atomic force microscopy indentation was used through microscale probing of multiple human breast cancer cells (MCF-7, MDA-MB-231), and human normal mammary epithelial cells (MCF-10A), under different levels of glycemic stress. These were used to study both benign and malignant breast tissue behaviors. Benign cells (MCF-10A) recorded higher Young’s modulus values than malignant cells (MCF-7 and MDA-231) under normoglycemic conditions, which agrees with the current literature. Moreover, exposure to high glucose (for 48 hours) decreased Young’s modulus in both benign and malignant cells, to the effect that the cancer cells showed a complete loss in elasticity with high glucose. This provides a possible insight into a link between glycemic stress and cytoskeletal strength. This work suggests that reducing glycemic stress in cancer patients and those at risk can prove beneficial in restoring normal cytoskeletal structure.

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.

scholarly journals NLRP3 as Putative Marker of Ipilimumab-Induced Cardiotoxicity in the Presence of Hyperglycemia in Estrogen-Responsive and Triple-Negative Breast Cancer Cells

2020 ◽  
Vol 21 (20) ◽  
pp. 7802 ◽  
Author(s):  
Vincenzo Quagliariello ◽  
Michelino De Laurentiis ◽  
Stefania Cocco ◽  
Giuseppina Rea ◽  
Annamaria Bonelli ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Triple Negative Breast Cancer ◽  
High Glucose ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Anticancer Efficacy ◽  
Low Glucose ◽  
Mcf 7

Hyperglycemia, obesity and metabolic syndrome are negative prognostic factors in breast cancer patients. Immune checkpoint inhibitors (ICIs) have revolutionized cancer treatment, achieving unprecedented efficacy in multiple malignancies. However, ICIs are associated with immune-related adverse events involving cardiotoxicity. We aimed to study if hyperglycemia could affect ipilimumab-induced anticancer efficacy and enhance its cardiotoxicity. Human cardiomyocytes and estrogen-responsive and triple-negative breast cancer cells (MCF-7 and MDA-MB-231 cell lines) were exposed to ipilimumab under high glucose (25 mM); low glucose (5.5 mM); high glucose and co-administration of SGLT-2 inhibitor (empagliflozin); shifting from high glucose to low glucose. Study of cell viability and the expression of new putative biomarkers of cardiotoxicity and resistance to ICIs (NLRP3, MyD88, cytokines) were quantified through ELISA (Cayman Chemical) methods. Hyperglycemia during treatment with ipilimumab increased cardiotoxicity and reduced mortality of breast cancer cells in a manner that is sensitive to NLRP3. Notably, treatment with ipilimumab and empagliflozin under high glucose or shifting from high glucose to low glucose reduced significantly the magnitude of the effects, increasing responsiveness to ipilimumab and reducing cardiotoxicity. To our knowledge, this is the first evidence that hyperglycemia exacerbates ipilimumab-induced cardiotoxicity and decreases its anticancer efficacy in MCF-7 and MDA-MB-231 cells. This study sets the stage for further tests on other breast cancer cell lines and primary cardiomyocytes and for preclinical trials in mice aimed to decrease glucose through nutritional interventions or administration of gliflozines during treatment with ipilimumab.

scholarly journals Evaluation of Potential Mechanisms Controlling the Catalase Expression in Breast Cancer Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Christophe Glorieux ◽  
Juan Marcelo Sandoval ◽  
Nicolas Dejeans ◽  
Sandrine Nonckreman ◽  
Khadija Bahloula ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Posttranslational Modifications ◽  
Breast Cancer Cells ◽  
Mammary Epithelial Cells ◽  
Dna Lesions ◽  
Mrna Levels ◽  
Chromosome 11 ◽  
Catalase Protein ◽  
Mcf 7

Development of cancer cell resistance against prooxidant drugs limits its potential clinical use. MCF-7 breast cancer cells chronically exposed to ascorbate/menadione became resistant (Resox cells) by increasing mainly catalase activity. Since catalase appears as an anticancer target, the elucidation of mechanisms regulating its expression is an important issue. In MCF-7 and Resox cells, karyotype analysis showed that chromosome 11 is not altered compared to healthy mammary epithelial cells. The genomic gain ofcatalaselocus observed in MCF-7 and Resox cells cannot explain the differential catalase expression. Since ROS cause DNA lesions, the activation of DNA damage signaling pathways may influence catalase expression. However, none of the related proteins (i.e., p53, ChK) was activated in Resox cells compared to MCF-7. The c-abl kinase may lead to catalase protein degradation via posttranslational modifications, but neither ubiquitination nor phosphorylation of catalase was detected after catalase immunoprecipitation. Catalase mRNA levels did not decrease after actinomycin D treatment in both cell lines. DNMT inhibitor (5-aza-2′-deoxycytidine) increased catalase protein level in MCF-7 and its resistance to prooxidant drugs. In line with our previous report, chromatin remodeling appears as the main regulator of catalase expression in breast cancer after chronic exposure to an oxidative stress.

scholarly journals Identification of Molecular Basis for Objective Discrimination of Breast Cancer Cells (MCF-7) from Normal Human Mammary Epithelial Cells by Raman Microspectroscopy and Multivariate Curve Resolution Analysis

2021 ◽  
Vol 22 (2) ◽  
pp. 800
Author(s):  
Keita Iwasaki ◽  
Asuka Araki ◽  
C Murali Krishna ◽  
Riruke Maruyama ◽  
Tatsuyuki Yamamoto ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Multivariate Curve Resolution ◽  
Human Mammary Epithelial ◽  
Resolution Analysis ◽  
Raman Spectral ◽  
Mcf 7

Raman spectroscopy (RS), a non-invasive and label-free method, has been suggested to improve accuracy of cytological and even histopathological diagnosis. To our knowledge, this novel technique tends to be employed without concrete knowledge of molecular changes in cells. Therefore, identification of Raman spectral markers for objective diagnosis is necessary for universal adoption of RS. As a model study, we investigated human mammary epithelial cells (HMEpC) and breast cancer cells (MCF-7) by RS and employed various multivariate analyses (MA) including principal components analysis (PCA), linear discriminant analysis (LDA), and support vector machine (SVM) to estimate diagnostic accuracy. Furthermore, to elucidate the underlying molecular changes in cancer cells, we utilized multivariate curve resolution analysis–alternating least squares (MCR-ALS) with non-negative constraints to extract physically meaningful spectra from complex cellular data. Unsupervised PCA and supervised MA, such as LDA and SVM, classified HMEpC and MCF-7 fairly well with high accuracy but without revealing molecular basis. Employing MCR-ALS analysis we identified five pure biomolecular spectra comprising DNA, proteins and three independent unsaturated lipid components. Relative abundance of lipid 1 seems to be strictly regulated between the two groups of cells and could be the basis for excellent discrimination by chemometrics-assisted RS. It was unambiguously assigned to linoleate rich glyceride and therefore serves as a Raman spectral marker for reliable diagnosis. This study successfully identified Raman spectral markers and demonstrated the potential of RS to become an excellent cytodiagnostic tool that can both accurately and objectively discriminates breast cancer from normal cells.

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