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CD26/DPP-4: Type 2 Diabetes Drug Target with Potential Influence on Cancer Biology

Emi Kawakita1, Daisuke Koya2,3, Keizo Kanasaki1,3

  • 1Internal Medicine 1, Shimane University Faculty of Medicine, 89-1 Enya-cho, Izumo 693-8501, Japan.

Cancers
|June 2, 2021
PubMed

Insights

Dipeptidyl peptidase-4 (DPP-4) inhibitors, used for type 2 diabetes, may unexpectedly promote breast cancer metastasis and chemoresistance. This occurs through increased C-X-C motif chemokine 12, highlighting potential risks for diabetic cancer patients.

Area of Science:

  • Biochemistry
  • Oncology
  • Endocrinology

Background:

  • Dipeptidyl peptidase-4 (DPP-4/CD26) is a glycoprotein with diverse functions, including incretin hormone degradation.
  • DPP-4 inhibitors are established therapeutics for type 2 diabetes (T2DM), targeting blood glucose control.
  • The impact of DPP-4 inhibitors on tumor biology, particularly cancer progression, remains incompletely understood.

Purpose of the Study:

  • To investigate the potential adverse effects of DPP-4 inhibition on tumor biology.
  • To elucidate the mechanisms by which DPP-4 inhibition might influence cancer metastasis and chemoresistance.

Main Methods:

  • Preclinical studies examining the effects of DPP-4 suppression on tumor progression.
  • Analysis of DPP-4 inhibitor-induced changes in cancer cell behavior and molecular pathways.

Main Results:

  • DPP-4 inhibition was found to enhance breast cancer metastasis and chemoresistance.
  • This effect is mediated by an increase in the substrate C-X-C motif chemokine 12 (CXCL12).
  • The elevated CXCL12 subsequently induces epithelial-mesenchymal transition (EMT) in tumor cells.

Conclusions:

  • DPP-4/CD26 has critical roles beyond glucose regulation, with potential implications for cancer development.
  • DPP-4 inhibitors may have unfavorable effects on tumor biology, including promoting metastasis and chemoresistance.
  • The safety of DPP-4 inhibitors in diabetic patients with co-existing cancer requires further investigation and mechanistic understanding.
Keywords:
CXCL12DPP-4epithelial-mesenchymal transitionmetformintype 2 diabetes

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