Objective: Lung adenocarcinoma is a type of lung cancer that falls under the category of non-small cell carcinoma. Given its high incidence, it has attracted considerable attention. Zinc finger TRAF-type containing 1 (ZFTRAF1) was found in a two-hybrid yeast screening with muine galectin-3. However, the link between ZFTRAF1 and lung adenocarcinoma was unclear. This study aimed to explore the influencing mechanism of ZFTRAF1 on lung adenocarcinoma. Material and Methods: In this study, by silencing or overexpressing ZFTRAF1, we investigated the migration and invasion ability of A549 and HCC827 cells. In addition, the polarization effect of ZFTRAF1 on macrophages was evaluated through flow cytometry and quantitative real-time polymerase chain reaction. Finally, tumor growth and development were evaluated through histological analysis in vivo and Western Blot analysis in vitro . Results: ZFTRAF1 was down-regulated in normal lung cells. Silencing of ZFTRAF1 inhibited migration, invasion of A549 and HCC827 cells, and the formation of tumors. Reduction of the expression of ZFTRAF1 inhibited the epithelial–mesenchymal transition, suppressed the phosphoinositide 3-kinase–protein kinase B pathway, and enhanced the polarization of M1 macrophages. In addition, the overexpression of ZFTRAF1 showed an opposite trend compared with its silencing in A549 and HCC827 cells. Conclusion: ZFTRAF1 promotes lung cancer development. Regulating the expression level of ZFTRAF1 to interfere with the growth and migration of lung adenocarcinoma may be a new strategy for the treatment of lung adenocarcinoma. In addition, the theoretical foundation for ZFTRAF1’s therapeutic use is provided in this work.
Yu et al. (Wed,) studied this question.