Gemcitabine promoting CCL2 secretion by Bladder cancer cell recruited MDSCs into tumor microenvironment
作者单位：Shanghai General Hospital
会议名称：《第十三届全国免疫学学术大会》
会议日期：2018年
学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学]
关 键 词：MDSCs Gemcitabine CCL2 Tumor microenvironment
摘 要：Background: Bladder cancer(BC) is one of the most common malignant tumors of the urinary tract in China, 75% to 85% of which are grouped as non-muscle invasive bladder ***(GEM), mainly known as chemotherapeutic drug, is known to enhance the resistance potential of cancer cells to ***, the mechanism of that remains *** of study: In this study, 5637 and T24 bladder cancer cell lines were divided into control groups and GEM treated *** cells treated drug concentration was tested by CCK-8 *** chemotaxis of MDSC from peripheral blood was evaluated by flow cytometry *** mRNA and protein level of CCL2 in BC cells was analyzed by qRT-PCR, ELISA and flow cytometry *** expression of the key molecules in GEM treated BC cells was assessed by in-cell Western *** effects of MDSCs on the proliferation of BC cells in vitro were assessed using flow cytometry ***: We have found that though GEM treatment can kill and wound BC cells, which leads to higher expression of CCL2 in the GEM treated groups than the control *** level of CCL2 significantly enhances the chemotaxis of MDSCs in the microenvironment of BC *** accumulation of MDSCs can promote the progression of BC, such as the proliferation, invasion and migration of the BC *** phenomenon can be inhibited by using CCR2 ***: GEM can enhance BC cells generate much more CCL2, which can recruit MDSC to tumor *** phenomenon can partly explain the mechanism of GEM related chemotherapy resistance.