Some IL-32 isoforms have been linked to disease outcome and were shown to positively influence tumor development and progression in various different malignancies, including gastric, breast and lung cancers.
Mechanistic studies indicated that TIMP-3 overexpression reduced NF-κB activity, which led to cell growth inhibition in IL-32γ transfected lung cancer cells.
Lymph node metastases frequently developed from IL-32-expressing lung cancers, and especially (82%) from those endowed with an IL-32-expressing leukocyte infiltrate (TIL) mainly composed of CD68(+) macrophages, CD4(+) T lymphocytes, and DC-SIGN(+) dendritic cells.