Nanoparticle-linked antagonist for leptin signaling inhibition in breast cancer
Nanoparticle-linked antagonist for leptin signaling inhibition in breast cancer作者机构：Department of Microbiology Biochemistry and Immunology Morehouse School of Medicine Department of Pathology and Laboratory Medicine Emory University School of Medicine
出 版 物：《World Journal of Clinical Oncology》 (世界临床肿瘤学杂志（英文版）)
年 卷 期：2017年第8卷第1期
页 面：54-66页
学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学]
基 金：The National Cancer Institute at the National Institutes of Health(1R41 CA183399-01A1 to Ruben R Gonzalez-Perez 5U54 CA118638,S21 MD000101,5G12 MD0076021,G12 RR026250-03,NIH RR03034 and 1C06 RR18386 to Morehouse School of Medicine) the National Institute of General Medical Sciences,Research Initiative for Scientific Enhancement Program(RISE 5R25 GM058268 to Tia Harmon) the Congressionally Directed Medical Research Programs-Department of Defense(CDMRP DOD W81XWH-13-1-0382 to Ruben R Gonzalez-Perez)
主 题：Triple negative breast cancer Obesity Leptin Leptin peptide receptor antagonist 2 Iron oxide nanoparticles Chemotherapy adjuvant
摘 要：AIM To develop a leptin peptide receptor antagonist linked to nanoparticles and determine its effect on viability of breast cancer *** The leptin antagonist, LPrA2, was coupled via EDAC [1-Ethyl-3-(3-dimethylaminopropyl)carbodiimide] to iron oxide nanoparticles(IONP-LPrA2) to increase its ***-LPrA2 conjugation was confirmed by Western blot and nanoparticle tracking *** triple negative breast cancer(TNBC) MDA-MB-231, HCC1806 and estrogen receptor positive(ER+) MCF-7 cells were analyzed for the expression of the leptin receptor, *** effects of leptin and antagonist on levels of leptin-induced STAT3 phosphorylation and cyclin D1, cell cycle progression, cell proliferation, and tumorsphere formation in breast cancer cells were *** of the chemotherapeutics [cisplatin(Cis), cyclophosphamide(CTX), doxorubicin(Dox) and paclitaxel(PTX)] to effectively reduce cell viability were *** effects of combination treatments of IONP-LPrA2 and chemotherapeutics on cell viability were *** Western blot analysis of coupling reaction products identified IONP-LPrA2 at approximately 100 ***2 significantly decreased leptin-induced p STAT3 levels in HCC1806 cells and drastically decreased cyclin D1 levels in all cell ***-LPrA2 significantly reduced leptin-induced S phase progression and cell proliferation in all breast cancer cell lines and the formation of tumorspheres in MDA-MB-231 ***, IONP-LPrA2 showed an additive effect on the reduction of breast cancer cell survival with *** plus IONP-LPrA2 produced a significant reduction in the survival of MDA-MB-231 and HCC1806 *** plus IONP-LPrA2 caused a significant decrease in the survival of MDA-MB-231 *** plus IONP-LPrA2 caused a marked reduction in the survival of HCC1806 ***, PTX plus IONP-LPrA2 did not have a major effect on the viability of the breast cancer cells when compared to PTX *** Prese
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