Blocking the Notch signal transduction pathway promotes tumor growth in breast cancer by promoting the expression of suppressible inflammatory factors.
机构：[1]Department of Animal Center, The Fourth Hospital of Hebei Medical University, Shijiazhuang, China医技科室实验动物中心河北医科大学第四医院[2]Hebei Provincial Key Laboratory of Tumor Microenvironment and Drug Resistance, Hebei Medical University, Shijiazhuang, China[3]School of Basic Medicine, Hebei Medical University, Shijiazhuang, China[4]Department of Hematology, The Fourth Hospital of Hebei Medical University, Shijiazhuang, China临床科室血液内科河北医科大学第四医院[5]Department of Radiotherapy, The Fourth Hospital of Hebei Medical University, Shijiazhuang, China河北医科大学第四医院[6]Research Center, The Fourth Hospital of Hebei Medical University, Shijiazhuang, China河北医科大学第四医院[7]Department of Breast Center, The Fourth Hospital of Hebei Medical University, Shijiazhuang, China河北医科大学第四医院
Breast cancer is the most common malignant tumor among all female tumors. It seriously affects the health and lives of patients, and poses a significant economic burden. The study of the molecular mechanisms of breast cancer occurrence, proliferation and growth and development is of great clinical significance.Notch1 knockout mice were obtained by gene targeting. The expression of inflammatory factor arginase-1 in each group of tumors was observed by immunofluorescence staining. Semi-quantitative detection of Notch1, Arginase-1, and proteins belonging to the PI3K-AKT pathway by western blot. The expression level of interleukin-3 (IL-3), and IL-4 in serum was quantified by enzyme linked immunosorbent assay (ELISA).In this study, Notch1 knockout in mice promoted the cell proliferation of breast cancer. Further study on molecular mechanisms demonstrated that the increased cell proliferation resulted from the activation of the PI3K-AKT signal transduction pathway. In addition, the expression of the M2-type inflammatory factor arginase-1 significantly increased, which was dependent on the activation of the PI3K-AKT pathway, indicating that Notch1 knockout in mice promoted the polarization of tumor-associated macrophages (TAMs). Consistent with this, IL-3 and IL-4 expression also significantly increased in the serum of Notch1 knockout mice.According to our results, Notch1 knockout in mice significantly promoted the cell proliferation of breast cancer, not only by activating the PI3K-AKT pathway, but also by promoting the polarization of TAMs towards the M2-type phenotype.2022 Annals of Translational Medicine. All rights reserved.
第一作者机构：[1]Department of Animal Center, The Fourth Hospital of Hebei Medical University, Shijiazhuang, China[2]Hebei Provincial Key Laboratory of Tumor Microenvironment and Drug Resistance, Hebei Medical University, Shijiazhuang, China
通讯作者：
通讯机构：[2]Hebei Provincial Key Laboratory of Tumor Microenvironment and Drug Resistance, Hebei Medical University, Shijiazhuang, China[7]Department of Breast Center, The Fourth Hospital of Hebei Medical University, Shijiazhuang, China[*1]Department of Breast Center, The Fourth Hospital of Hebei Medical University, Shijiazhuang 050011, China.
推荐引用方式(GB/T 7714)：
Ren Shuguang,Hu Yueyang,Ju Yingchao,et al.Blocking the Notch signal transduction pathway promotes tumor growth in breast cancer by promoting the expression of suppressible inflammatory factors.[J].ANNALS OF TRANSLATIONAL MEDICINE.2022,10(6):doi:10.21037/atm-22-1041.
APA：
Ren Shuguang,Hu Yueyang,Ju Yingchao,Sang Yang,Wu Jianhua...&Liu Yunjiang.(2022).Blocking the Notch signal transduction pathway promotes tumor growth in breast cancer by promoting the expression of suppressible inflammatory factors..ANNALS OF TRANSLATIONAL MEDICINE,10,(6)
MLA：
Ren Shuguang,et al."Blocking the Notch signal transduction pathway promotes tumor growth in breast cancer by promoting the expression of suppressible inflammatory factors.".ANNALS OF TRANSLATIONAL MEDICINE 10..6(2022)
