Anti-TRIM59 (aa 253-302) polyclonal antibody

Aberrant expression of the tripartite motif containing 59 (TRIM59) has been reported to participate in the development and progression of various human cancers. However, its expression pattern and cellular roles in pancreatic cancer (PC) remains unclear. In our study, we found that TRIM59 expression was significantly increased in PC tissues and was positively correlated with several malignant behaviors and poor overall survival of PC patients based on bioinformatics analysis and immunohistochemistry staining. Functionally, small interfering RNA-mediated TRIM59 depletion inhibited cell proliferation and migration in vitro, while TRIM59 overexpression promoted cell proliferation and migration in vitro and drove tumor growth and liver metastasis in vivo. Mechanically, TRIM59 was found to enhance glycolysis through activating the PI3K/AKT/mTOR pathway, ultimately contributing to PC progression. Taken together, our results demonstrate that TRIM59 may be a potential predictor for PC and promotes PC progression via the PI3K/AKT/mTOR-glycolysis signaling pathway, which establishes the rationale for targeting the TRIM59-related pathways to treat PC.

Ovarian cancer is the fifth common cause of death in woman worldwide. The tripartite motif-containing (TRIM) proteins consist of more than 70 known protein members. Studies have showed that TRIM proteins are involved in cancer and play important roles in cancer cell proliferation, migration, adhesion and metastasis. Recent studies have indicated that TRIM59, as a putative ubiquitin ligase, is up-regulated in some cancers and associated with poor prognosis of gastric cancer. However, the exact roles of TRIM59 in ovarian cancer are still unknown. In this study, we found that TRIM59 expression was increased and positively associated with histological grades (P = 0.000), FIGO stages (P = 0.016), and metastasis (P = 0.027) in ovarian cancer. A integrative data analysis tool revealed that ovarian cancer patients with high TRIM59 expression were correlated with more unfavorable overall and progression-free survival than the rest patients with low TRIM59 expression (P = 0.0024 and P = 7.5x10(-6), respectively). Based on the finding in the clinical data, we performed a series of cell line and animal experiments, and found that TRIM59 knockdown could significantly inhibit the ovarian cancer cell proliferation, clone formation, and invasion in vitro and the ovarian cancer growth of the subcutaneous and orthotopic implantation in vivo. Furthermore, TRIM59 was found to interact with Annexin A2 and induce Annexin A2 expression. Our data imply that TRIM59 can serve as a promising prognostic marker and a potential therapeutic target.