Carboxypeptidase A4 (CPA4) is a zinc-containing metallocarboxypeptidase. It belongs to the metallocarboxypeptidase family and may be involved in the modulation of peptide hormone activity and hormone-regulated tissue growth and differentiation. In various cancers, it has been associated with pathways like PI3K-AKT-mTOR, which is crucial for cell growth, survival, and metabolism [3,6].

In clear cell renal cell carcinoma (ccRCC), CPA4 is overexpressed, and higher expression is linked to worse clinical outcomes such as TNM stage, pathological stage, and histological grade, along with poorer survival rates [1]. In pancreatic cancer, overexpression of CPA4 promotes epithelial-to-mesenchymal transition (EMT) via stimulating the PI3K-AKT-mTOR signaling, and is related to tumor size, T stage, lymph-node metastasis, and a worse prognosis [3]. In non-small-cell lung cancer (NSCLC), circular RNA circ-CPA4 regulates cell growth, stemness, drug resistance, and immune evasion through the let-7 miRNA/PD-L1 axis [2]. Also, knockdown of CPA4 inhibits NSCLC cell growth by suppressing the AKT/c-MYC pathway [5]. In endometrial cancer, CPA4 is significantly overexpressed, correlating with tumor progression and poor prognosis, and reducing it in cell lines inhibits tumor growth and spread [4]. In gastric cancer, knockdown of CPA4 inhibits cell colony formation, proliferation, migration, and invasion, and promotes apoptosis via cell cycle arrest and EMT inhibition [6].

In conclusion, CPA4 is highly relevant in multiple cancer types. Its overexpression often promotes cancer progression, including processes like cell proliferation, migration, metastasis, and EMT. The functional studies, especially those through knockdown or knockout-like experiments in cell lines, help reveal its oncogenic roles in various cancers, providing potential biomarker and therapeutic target candidates for these diseases.