D Pathophysiology, College of Fundamental Medical Sciences, Wuhan University, Wuhan, Hubei, ChinaDepartment of Anatomy, School

D Pathophysiology, College of Fundamental Medical Sciences, Wuhan University, Wuhan, Hubei, ChinaDepartment of Anatomy, School of Standard Medical Sciences, Wuhan University, Wuhan, Hubei, ChinaHubei Crucial Laboratory of Tumor Biological Behaviors, Division of Breast and Thyroid Surgery, Hubei Cancer Clinical Study Center, Zhongnan Hospital, Wuhan University, Wuhan, Hubei, China Correspondence Lei Wei, Department of Pathology and Pathophysiology, Hubei Provincial Essential Laboratory of Developmentally Originated Disease, College of Basic Healthcare Sciences, Wuhan University, Wuhan, Hubei, China. Email: [email protected] Funding info National Natural Science Foundation of China, GrantAward Number: 81572943 andAbstract Breast cancer was the highest incidence of tumor in ladies, which seriously threaten women’s overall health. Our prior study located that the expression of IQUB (IQ motif and ubiquitin domain containing) was drastically enhanced in the development of breast cancer by transcriptome sequencing. Nonetheless, there have been no research around the mechanism of IQUB in tumorigenesis. Further study showed that IQUB expression was significantly improved in breast cancer, which had a drastically good correlation with pathological differentiation of breast cancer by tissue microarray evaluation. Furthermore, we also found that IQUB overexpression could definitely promote the proliferation and migration of MCF7 cells and boost the proportion of MCF7 cells in S and G2M phase in vitro study, even though knockdown of IQUB brought on inhibition of cell proliferation and migration in MDAMB231 cells and improved the proportion of MDAMB231 cells in G1 phase. Moreover, IQUB overexpression or knockdown combined with treatment of Licl or MG132 showed that IQUB activated Akt to promote GSK3 phosphorylation, which in turn activated Phosphonoacetic acid Endogenous Metabolite Wntcatenin signaling pathway in breast cancer cells. Taken collectively, these results indicated that upregulated IQUB promoted breast cancer cell proliferation and migration via activating AktGSK3catenin signaling pathway, which played an essential element within the tumorigenesis and development of breast cancer.Keyword phrases AktGSK3catenin signaling pathway, breast cancer, cell migration, cell proliferation, IQ motif and ubiquitin domain containingIN T RO D U C T IONAccording to the Tumor Epidemiology Survey in 2017, breast cancer has become the highest incidence of women’s cancerKai Li, Yanbin Ma and Zun Zhang equally contributed to this study.in American, which seriously impacts the well being of ladies.1 In China, there was an estimated 0.27 million breast cancer situations which leaded to 0.07 million deaths in 2015.2 Breast cancer individuals mostly died of cancer metastasis; having said that,This really is an open access report below the terms of the Inventive Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is effectively cited. 2018 The Authors. Cancer Medicine published by John Wiley Sons Ltd. Cancer Medicine. 2018;7:3875888. wileyonlinelibrary.comjournalcamLI et aL.the mechanism of breast cancer cells proliferation and metastasis was not clear, which Methoxyacetic acid Description needed additional study. Decades of studies had discovered that there was a close correlation involving the development of breast cancer as well as the activation of oncogenic signaling pathway, including Wntcatenin signaling pathway, triggered by the inactivation of tumor suppressor gene or the activation of oncogene.three Consequently, seeking new oncogenes and their related signal.