Protein regulator of cytokinesis 1 regulates autophagy in hepatitis B virus‑associated liver cancer development.

Hepatitis B protein x (HBx) is considered a critical contributor to hepatitis B virus (HBV)‑associated liver cancer development. Protein regulator of cytokinesis 1 (PRC1) has been implicated in hepatocarcinogenesis. However, the clinical relevance, biological functions and related regulatory mechanisms of PRC1 in HBV‑associated liver cancer have not yet been clarified. PRC1 expression profiles in liver cancer were obtained from The Cancer Genome Atlas and Gene Expression Profiling Interactive Analysis database and through reverse transcription‑quantitative polymerase chain reaction and immunohistochemistry assays. A series of in vitro and in vivo assays were used to explore the function of the PRC1 gene and the possible mechanisms through which it affects HBV‑associated liver cancer. PRC1 was overexpressed in HBV‑positive liver cancer tissues. Functional studies in vitro demonstrated that HBx induced the expression of the PRC1 gene, which promoted cell autophagy and enhanced viability, invasion and migration. Furthermore, the knockdown of the PRC1 gene or treatment with the autophagosome inhibitor 3‑methyladenine blocked the HBx‑induced autophagic flux, disrupted the formation of autophagosomes, and promoted cell apoptosis. Liver cancer xenograft animal model experiments revealed that inhibition of autophagy by 3‑methyladenine or silencing of the PRC1 gene attenuated HBx‑induced malignant behavior in vivo . The absence of autophagy inhibited the expression of Bcl‑2, induced the expression of Bax, and regulated the levels of Th1 and Th2 cytokines. These results elucidate a mechanism wherein the PRC1 gene participates in the occurrence and development of HBV‑associated liver cancer by modulating autophagy. PRC1 could be a potential therapeutic target for liver cancer.