Recombinant human PDCD5 exhibits an antitumor role in hepatocellular carcinoma cells via clathrin‑dependent endocytosis.

Liver cancer is the fifth most frequently diagnosed type of cancer in men worldwide. Recombinant human programmed cell death 5 (rhPDCD5) has been shown to enter a variety of cells by clathrin-independent endocytosis. Tissue specimens from 32 hepatocellular carcinoma (HCC) patients were collected for analysis of PDCD5 expression using ELISA. It was confirmed that the pre-operative serum levels of PDCD5 protein in patients with HCC were significantly lower than the post-operative serum levels. Moreover, the serum PDCD5 levels were significantly correlated with portal invasion and lymph node metastasis. rhPDCD5 inhibited cell proliferation as indicated by an MTT assay, and induced apoptosis and S-phase arrest in HCC cells as demonstrated by flow cytometric analysis. Furthermore, rhPDCD5 suppressed tumor growth in established xenograft tumor models. In addition, Pitstop2 was used to block clathrin-dependent endocytosis (CDE), which confirmed that the anti-tumor effect of rhPDCD5 in HCC cells is mediated via CDE.