BAG2 Promotes Proliferation and Metastasis of Gastric Cancer via ERK1/2 Signaling and Partially Regulated by miR186

Lisha Sun; Guanglei Chen; Anqi Sun; Zheng Wang; Haibo Huang; Ziming Gao; Weitian Liang; Caigang Liu; Kai Li

doi:10.3389/fonc.2020.00031

BAG2 Promotes Proliferation and Metastasis of Gastric Cancer via ERK1/2 Signaling and Partially Regulated by miR186

Front Oncol. 2020 Jan 31:10:31. doi: 10.3389/fonc.2020.00031. eCollection 2020.

Authors

Lisha Sun¹, Guanglei Chen², Anqi Sun¹, Zheng Wang³, Haibo Huang¹, Ziming Gao¹, Weitian Liang¹, Caigang Liu², Kai Li¹

Affiliations

¹ Department of Surgical Oncology, The First Hospital of China Medical University, Shenyang, China.
² Department of Breast Surgery, Shengjing Hospital of China Medical University, Shenyang, China.
³ Department of Otorhinolaryngology, The First Hospital of China Medical University, Shenyang, China.

Abstract

Bcl2-associated athanogene (BAG)2 as a co-chaperone has been demonstrated to be involved in tumor growth and metastasis, but its biological function in gastric cancer remains unknown. Here, we reported that BAG2 was highly expressed in gastric cancer cell lines and tissues, indicating poor prognosis. High expression of BAG2 was significantly associated with T stage and differentiation level of gastric cancer (P < 0.001). Functional experiments revealed that BAG2 knockdown in gastric cancer cells inhibited the proliferation, invasion and migration of cells through AKT/mTOR and extracellular regulated kinase (ERK) pathways. Proteomic analysis identified that BAG2 may be involved in the regulation of mitogen-activated protein kinase (MAPK) pathway. In addition, immunoprecipitation showed that BAG2 could bind to ERK1/2. Luciferase reporter assay and Western blot verified that BAG2 was down-regulated by miR186. Taken together, our findings may reveal the basic function of BAG2 and uncover a potential therapeutic target for gastric cancer.

Keywords: BAG2; gastric cancer; iTRAQ proteomics technology; miR186; therapeutic target.