Dipeptidyl peptidase III (DPP3), a zinc‑dependent
metallopeptidase, is upregulated in a variety of
malignancies. However, little is known about its roles in the pathogenesis of these
malignancies. The present study was designed to investigate the roles of DPP3 in the pathogenesis and progression of oesophageal
cancer (EC). The expression level of DPP3 in EC tissues and adjacent normal tissues was detected in 93 cases of tissue biopsies collected from patients diagnosed with oesophageal
carcinoma by immunohistochemistry. The effect of DPP3 expression on cell proliferation, migration or apoptosis was determined in DPP3‑depleted EC cells created by
infection with lentivirus containing
short hairpin RNA specific to the human DPP3
mRNA sequence, followed by detection at the cellular level using a Celigo cell count assay, flow cytometry, wound‑healing assay and Transwell assay as well as chip screening with a Human Apoptosis Antibody Array kit, which enables the quantitative detection of 43 apoptosis‑related genes. A xenograft model was applied to detect the tumour growth and invasion of DPP3‑depleted
cancer cells in nude mice. The results revealed that DPP3 expression was elevated in EC tissues compared with adjacent non‑tumour tissues, and high DPP3 expression was significantly associated with poor prognosis. DPP3 depletion resulted in reduced cell proliferation and migration and enhanced cell cycle arrest and apoptosis of EC cells and led to the inhibition of tumour growth and invasion in a xenograft model. 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.