Interleukin-22 promotes triple negative breast cancer cells migration and paclitaxel resistance through JAK-STAT3/MAPKs/AKT signaling pathways

Abstract

PurposeOwing to the absence of any targeted therapies, triple negative breast cancer (TNBC), which accounts for approximately 15% of all breast cancers, typically have a poorer outcome. In an attempt to find out the TNBCs' microenvironment, we ran into the endogenous expression of a newly discovered cytokine known as Interleukin (IL)-22. MethodsThirty TNBC patients were recruited and the levels of IL-22 producing (Th22) cells in tumor, paratumor and normal breast tissues were measured. Then we studied the role and mechanism of IL-22 in migration and paclitaxel resistance in TNBC cells MDA-MB 468 and MDA-MB 231. ResultsThe prevalence of Th22 cells were gradually increased in normal, paratumor and tumor tissues. In vitro, IL-22 promotes TNBC cells migration and induces paclitaxel resistance. Importantly, IL-22 exposure of TNBC cells resulted in JAK-STAT3/MAPKs/AKT signaling pathways activated. ConclusionIL-22 may play an accelerating role in the development of TNBC and may open a new therapeutic approach for TNBC.