乳腺癌
癌细胞
癌症
医学
糖尿病
转移
血糖性
内科学
细胞骨架
癌症研究
内分泌学
病理
细胞
肿瘤科
化学
生物化学
作者
Diganta Dutta,Xavier‐Lewis Palmer,Jose Ortega-Rodas,Vasundhara Balraj,Indrani Ghosh Dastider,Surabhi Chandra
出处
期刊:Breast cancer
[SAGE Publishing]
日期:2020-01-01
卷期号:14: 117822342097236-117822342097236
被引量:8
标识
DOI:10.1177/1178223420972362
摘要
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.
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