DPP3 (Dipeptidyl Peptidase 3)

Knocking down MICB could reverse the phenotypic changes induced by high DPP3 expression. Conclusion DPP3 inhibits the immune escape of gastric cancer cells by downregulating MICB expression.

This study demonstrates that DPP3 plays a role in the reprogramming of fatty acid metabolism in tumors and is associated with poor prognosis in breast cancer patients. These findings will provide a new therapeutic target for the treatment of breast cancer.

Additionally, DPP3 knockdown led to downregulation of the NRF2 pathway proteins, such as NRF2, G6PD, and NQO1 along with increased sensitivity towards oxidative stress-induced cell death and chemotherapy. Conclusively, these results demonstrate critical role of DPP3 in ESCC and DPP3/NRF2 axis may serve as an attractive therapeutic target against chemoresistance in this malignancy.

In addition, DPP3 depletion was associated with the upregulation of the proapoptotic proteins SMAC and p53 and the downregulation of the antiapoptotic proteins clAP‑2, IGFBP‑2 and TRAILR‑4. Finally, DPP3 may promote cell proliferation, migration and survival of EC cells in vitro and tumour growth and invasion of oesophageal carcinoma in vivo, and thus may serve as a molecular target for tumour therapy.

Overexpression of CDK1 alleviates the inhibitory effects of DPP3 knockdown in CRC cells. In summary, DPP3 has oncogene-like functions in the development and progression of CRC by targeting CDK1, which may be an effective molecular target for the prognosis and treatment of CRC.