Abstract:
:Macrophage migration inhibitory factor (MIF) is up-regulated in diverse solid tumors and acts as the critical link between immune response and tumorigenesis. In this study, we demonstrated that MIF overexpression promoted migration of breast cancer cells by elevating TLR4 expression. Further investigation evidenced that MIF induced ROS generation. MIF-induced ROS led to ERK phosphorylation, which facilitated HMGB1 release from the nucleus to the cytoplasm. MIF overexpression also induced caveolin-1 phosphorylation. Caveolin-1 phosphorylation contributed to HMGB1 secretion from the cytoplasm to the extracellular matrix. The extracellular HMGB1 activated TLR4 signaling including NF-κB phosphorylation, which was responsible for the transcription of Snail and Twist as well as MMP2 activation. Furthermore, MIF-induced caveolin-1-dependent HMGB1 secretion might control the recruitment of CD11b+ immune cells. Our data suggested that MIF affected the intrinsic properties of tumors and the host immune response in tumor microenvironment by regulating the TLR4/HMGB1 axis, leading to metastasis of breast cancer.
journal_name
Cancer Lettjournal_title
Cancer lettersauthors
Lv W,Chen N,Lin Y,Ma H,Ruan Y,Li Z,Li X,Pan X,Tian Xdoi
10.1016/j.canlet.2016.02.005subject
Has Abstractpub_date
2016-06-01 00:00:00pages
245-255issue
2eissn
0304-3835issn
1872-7980pii
S0304-3835(16)30051-9journal_volume
375pub_type
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