Background
Gastric cancer is one of the most prevalent cancers, with a low survival rate at the later stages. Carboxypeptidase A4 (CPA4) is associated with the aggressiveness and growth in cancer. However, its regulatory role in gastric cancer remains unknown. Therefore, we investigated the role of CPA4 in gastric cancer progression in vitro.
Conclusions
Knockdown of CPA4 inhibited cell progression via arresting the cell cycle and inducing EMT in gastric cancer.
Methods
The human gastric adenocarcinoma cell line (AGS cell line) was used in the present study. CPA4 knockdown lentiviruses were constructed. Western blot analysis was performed to evaluate the protein expression levels of epithelial-mesenchymal transition (EMT) transcription factors, EMT biomarkers, and proteins involved in the Wnt signaling pathway, mitogen-activated protein kinase (MAPK) signaling pathway, and phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway. Quantitative real-time polymerase chain reaction (qRT-PCR) analysis was carried out to evaluate the mRNA expression level of CPA4. The String database was employed for protein-protein interaction (PPI) network analysis. Cell colony formation, proliferation, migration, invasion, apoptosis, and cell cycle analyses were performed using corresponding kits.
Results
CPA4 is highly expressed in gastric cancer cell lines. Overexpressed CPA4 was associated with the induction of EMT. Knockdown of CPA4 inhibited cell colony formation, proliferation, migration, and invasion of gastric cancer cells. Knockdown of CPA4 also promoted cell apoptosis of gastric cancer cells. Conclusions: Knockdown of CPA4 inhibited cell progression via arresting the cell cycle and inducing EMT in gastric cancer.