Wednesday, June 6, 2018

PLGA from PolySciTech used in development of therapeutic nanoparticle system for treatment of diabetes-associated breast cancer



There are many causes and factors involved with cancer growth. One factor is abnormal levels of sugar resultant from diabetes. Since cancer cells have unusual metabolism, diabetes can encourage cancer to form or exacerbate existing cancers. Recently, researchers working at Tongji University, Shanghai Jiao Tong University, Charles R. Drew University, University of North Texas, University of Texas at Arlington, Xavier University of Louisiana, California State University, and University of California used PLGA from PolySciTech (www.polyscitech.com) to create nanoparticles for delivering a novel therapeutic drug which targets cancer’s dependence on glucose. This research holds promise to provide for better strategies to treat diabetes-associated breast cancer. Read more: Ke Wu, Xiaoting Yu, Zhimin Huang, Donghui Zhu, Xianghua Yi, Ying-Li Wu, Qiongyu Hao, Kevin T. Kemp II, Yahya Elshimali, Roshni Iyer, Kytai Truong Nguyen, Shilong Zheng, Guanglin Chen, Qiao-Hong Chen, Guangdi Wang, Jaydutt V Vadgama, and Yong Wu. "Targeting of PP2Cδ by a small molecule C23 inhibits high glucose-induced breast cancer progression in vivo". Antioxidants and Redox Signaling DOI: 10.1089/ars.2017.7486 (https://www.liebertpub.com/doi/abs/10.1089/ars.2017.7486).

“Abstract: Aims: Epidemiologic evidence indicates that diabetes may increase risk of breast cancer (BC) and mortality in patients with cancer. The pathophysiological relationships between diabetes and cancer are not fully understood and personalized treatments for diabetes-associated BC are urgently needed. Results: We observed that high glucose (HG), via activation of nuclear phosphatase PP2Cδ, suppresses p53 function and consequently promotes BC cell proliferation, migration and invasion. PP2Cδ expression is higher in tumor tissues from BC patients with hyperglycemia than those with normoglycemia. The mechanisms underlying HG stimulation of PP2Cδ involve classical/novel PKCs activation and GSK3β phosphorylation. Reactive oxygen species (ROS)/NF-κB pathway also mediates HG induction of PP2Cδ. Furthermore, we identified a 1,5-diheteroarylpenta-1,4-dien-3-one (C23) as a novel potent PP2Cδ inhibitor with a striking cytotoxicity on MCF-7 cells through cell-based screening assay for growth inhibition and activity of a group of curcumin mimics. Besides directly inhibiting PP2Cδ activity, C23 blocks HG induction of PP2Cδ expression via HSP27 induction and subsequent ablation of ROS/NF-κB activation. C23 thus can significantly block HG-triggered inhibition of p53 activity, leading to the inhibition of cancer cell proliferation, migration and invasion. Additionally, hyperglycemia promotes BC development in diabetic nude mice and C23 inhibits the xenografted BC tumor growth. Conclusions and Innovation: Our findings elucidate mechanisms that may have contributed to diabetes-associated breast cancer progression and provide the first evidence to support the possible alternative therapeutic approach to breast cancer patients with diabetes.”

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