NFκB/p65 activation is involved in regulation of rBTI-induced glucocorticoid receptor expression in MCF-7 cell lines

• The new function reports about recombinant buckwheat trypsin inhibitor (rBTI).
• rBTI could inhibit MCF-7 cell proliferation and block cell cycle at G2/M period.
• The regulation mechanism of rBTI of MCF-7 involves the NFκB/p65 pathway.
• NFκB/p65 activation is involved in regulation of rBTI-induced GR expression.

Buckwheat is a food and medicinal plant product. We have previously obtained a high purity recombinant buckwheat trypsin inhibitor (rBTI) by cloning, expression and one-step affinity purification. Herein, we investigated the effect of rBTI on MCF-7 cell proliferation, migration, cell cycle and apoptosis. Results showed that rBTI could inhibit cell growth, migration, and induce cell apoptosis through blocking the cell cycle, causing a loss of mitochondrial transmembrane potential which results in caspase-dependent apoptosis in breast cancer cells. Mechanistically, rBTI could activate NFκB in MCF-7 cells by promoting the phosphorylation of IKKα/β and IκBα, inducing p65 nuclear translocation and increasing the ROS generation. rBTI also could promote the nuclear GR expression by activating the NFκB/p65 pathway. It demonstrated that NFκB/p65 activation is involved in the regulation of rBTI-induced glucocorticoid receptor expression in MCF-7 cell lines. Taken together, the rBTI may be exploited as a therapeutic agent against breast cancer metastasis.