STIP1 Regulates Proliferation and Migration of Lung Adenocarcinoma Through JAK2/STAT3 Signaling Pathway

Recent studies have shown that STIP1 is associated with proliferation and migration in numerous types of tumors; however, the role of STIP1 in lung adenocarcinoma is still poorly understood. Therefore, the aim of this study was to evaluate the role of STIP1 in lung adenocarcinoma, in vitro and in vivo.

The expression of STIP1 in lung adenocarcinoma was assessed by immunohistochemistry, RT-qPCR, and Western blot. The effects of STIP1 on the proliferation of lung adenocarcinoma cells were detected by the cell counting kit-8 assay; the effect of STIP1 on adhesion of lung adenocarcinoma cells was detected by Giemsa staining, while the cell scratch and Transwell assays were employed to examine the effect of STIP1 on the migratory ability of lung adenocarcinoma cells. Finally, apoptosis was evaluated by Hoechst staining and flow cytometry.

The expression level of STIP1 in lung adenocarcinoma tissue was significantly higher than that in adjacent normal tissue (P<0.05). Compared with that in nontransfected controls, cell proliferation, adhesion, and migration, as well as vimentin protein expression and levels of phosphorylated JAK2/STAT3, were significantly decreased (P<0.05) in A549 lung adenocarcinoma cells transfected with STIP1 shRNA, whereas E-cadherin protein expression and rates of apoptosis were significantly increased in these cells (P< 0.05).

Elevated expression of STIP1 in lung adenocarcinoma may enhance the proliferative, adhesive, and migratory ability, and reduce the apoptosis of lung adenocarcinoma cells through the JAK2/STAT3 signaling pathway and epithelial-mesenchymal transition (EMT), thereby promoting the recurrence and metastatic potential of this cancer. The results indicate that STIP1 may be an effective therapeutic target for the treatment of lung adenocarcinoma.