FAM49B promotes breast cancer proliferation, metastasis, and chemoresistance by stabilizing ELAVL1 protein and regulating downstream Rab10/TLR4 pathway

作者：Yanhui Li, Yue Xiong, Zhen Wang, Jianjun Han, Sufang Shi, Jinglan He, Na Shen, Wenjuan Wu, Rui Wang, Weiwei Lv, Yajun Deng, Weiguang Liu · 发表于：Cancer Cell International · 年份：2021 · DOI：10.1186/s12935-021-02244-9 · 被引用次数：31 · 研究领域：Cell Adhesion Molecules Research、Cardiovascular, Neuropeptides, and Oxidative Stress Research、Advanced Glycation End Products research

BACKGROUND: Breast cancer (BC) is one of the most common cancers and the leading cause of death in women. Previous studies have demonstrated that FAM49B is implicated in several tumor progression, however, the role and mechanism of FAM49B in BC remain to be explored. Therefore, in this study, we aimed to systematically study the role of FAM49B in the proliferation, metastasis, apoptosis, and chemoresistance of BC, as well as the corresponding molecular mechanisms and downstream target. METHODS: The ONCOMINE databases and Kaplan-Meier plotter databases were analyzed to find FAM49B and its prognostic values in BC. FAM49B expression in BC and adjacent non-tumor tissues was detected by western blot and IHC. Kaplan-Meier analysis was used to identify the prognosis of BC patients. After FAM49B knockdown in MCF-7 and MDA-MB-231 cells, a combination of co-immunoprecipitation, MTT, migration, and apoptosis assays, nude mouse xenograft tumor model, in addition to microarray detection and data analysis was used for further mechanistic studies. RESULTS: In BC, the results showed that the expression level of FAM49B was significantly higher than that in normal breast tissue, and highly expression of FAM49B was significantly positively correlated with tumor volume, histological grade, lymph node metastasis rate, and poor prognosis. Knockdown of FAM49B inhibited the proliferation and migration of BC cells in vitro and in vivo. Microarray analysis revealed that the Toll-like receptor signalin...