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. 2021 May 2;13(9):2191. doi: 10.3390/cancers13092191

Figure 1.

Figure 1

The impact of DPP-4 inhibitor on mammary tumor via CXCL12/CXCR4 downstream pathway. (A) DPP-4 digests CXCL12 for enzymatic action, thus the CXCL12-mediated CXCR4 downstream pathway in cancer is not strongly activated in the presence of DPP-4. (B) The DPP-4 inhibitor suppresses the degradation of CXCL12 and increases the level of CXCL12. Elevated CXCL12 interacts with its receptor CXCR4 and induces mTOR activation. The DPP-4 inhibitor-induced CXCL12/CXCR4/mTOR pathway causes mammary tumor proliferation. The activation of mTOR also causes EMT, which induces metastasis and chemoresistance in the mammary tumor. CXCL12: C-X-C motif chemokine 12; CXCR4: C-X-C receptor 4; DPP-4: dipeptidyl peptidase-4; EMT: epithelial-mesenchymal transition; mTOR: mammalian target of rapamycin.