Additionally, expression of the beta-transcript could be suppressed when CSC-enriched cells were treated with the BET-bromodomain inhibitor JQ1...Additionally, IL32 suppression decreased the invasiveness of SUM159PT based on an ECM-matrix cell invasion assay. Collectively, our results reflect the notion that differential IL32 expression by promoter hypomethylation in breast CSCs plays a role in ECM remodeling for purposes of breast cancer cell invasion and metastasis.
Taken together, our results indicated that EV-IL-32 derived from ESCC cell line could be internalized by macrophages and lead to M2 macrophage polarization via FAK-STAT3 pathway, thus promoting the metastasis of ESCC. These findings indicated that IL-32 could serve as a potential therapeutic target in patients with ESCC.