Magic™ Anti-CD79A monoclonal antibody, clone IM58 (1).

Recently, increasing evidence has revealed that long noncoding RNAs (lncRNAs) play important roles in the pathogenesis of multiple cancers. Although the oncogenic effects of lncRNA nuclear-enriched abundant transcript 1 (NEAT1) in some cancers have been reported, the functional significance and molecular mechanism of NEAT1 in pancreatic cancer (PC) progression remains elusive. In this study, our findings showed that NEAT1 expression was upregulated in PC tissues and cell lines; high NEAT1 expression was associated with tumor size, TNM stage, lymph node and distant metastasis, and also predicted poor prognosis. Functional experiments demonstrated that NEAT1 could promote PC cell proliferation and metastasis both in vitro and in vivo. Mechanistically, NEAT1 could associate with E74 like ETS transcription factor 3 (ELF3) mRNA and enhance the combination of Insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) and ELF3 mRNA, subsequently suppressing the degradation of ELF3 mRNA. Overall, our research indicates that NEAT1 might be a potential therapeutic target for patients with PC.

ELF3 is one of the member of transcription factors from E-twenty-six family, its role varies in different types of cancer. However, the role and specific mechanisms of ELF3 in the development of non-small cell lung cancer (NSCLC) still remains largely unknown. In our study, ELF3 was observed to be upregulated in NSCLC tissues compared to the corresponding normal lung tissue at mRNA and protein levels, and its expression level was correlated with the overall survival of patients with NSCLC. Silencing of the ELF3 gene in NSCLC cells inhibited the proliferation and metastasis significantly in vitro and in vivo. Conversely, overexpression of ELF3 in NSCLC cells promoted cancer growth and metastasis in vitro. Mechanistically, ELF3 activated PI3K/AKT and ERK signaling pathways and its downstream effectors, thus regulating the cell cycle and epithelial-mesenchymal transition (EMT). Furthermore, the promotive effects of ELF3 on cellular proliferation and metastasis could be rescued by Ly294002 (inhibitor of PI3K) and U0126 (inhibitor of MEK1/2). The results show that ELF3 promotes cell growth and metastasis by regulating PI3K/Akt and ERK pathways in NSCLC and that it may be a promising new target for the treatment of NSCLC patients.