Interleukin-32 contributes to invasion and metastasis of primary lung adenocarcinoma via NF-kappaB induced matrix metalloproteinases 2 and 9 expression

•Interleukin(IL)-32 was overexpressed in lung adenocarcinoma tissues and cell lines.•IL-32 expression correlated with tumor metastasis, and leads to poor prognosis.•Ectopic expression of IL-32 facilitated invasion and migration of tumor cells.•IL-32-induced metastasis was via MMP2 and MMP9 upregulation through NF-κB pathway.

Interleukin (IL)-32 is a novel proinflammatory cytokine, which has been shown to play an important role in tumor growth and metastasis. Here, we discovered that IL-32 was aberrantly over-expressed in lung adenocarcinoma tissues and cell lines. Positive expression of IL-32 significantly correlated with the clinical staging, and lymph node and distant metastases. High expression of IL-32 was an independent indicator of poor prognosis in lung adenocarcinoma patients. Moreover, IL-32-facilitated cell migration and invasion in vitro was mediated through transactivation of the nuclear transcription factor (NF)-κB signaling pathway and subsequent upregulation of matrix metalloproteinase (MMP)-2 and MMP9 expression. These studies demonstrate that IL-32 plays a role in the tumor-associated inflammatory microenvironment and that overexpression of IL-32 contributes to invasion and metastasis in primary lung adenocarcinoma, suggesting that it may have clinical utility as a prognostic biomarker and potential target for immunotherapy in lung adenocarcinoma.