C‑Myc‑regulated RPLP0 via the ROS‑mediated JAK2/STAT3 positive feedback loop facilitates hepatocellular carcinoma malignancy progression.

ABSTRACT: Hepatocellular carcinoma (HCC) continues to rank as a predominant contributor to cancer‑related mortality on a global scale, attributed to its insidious onset and unfavorable prognosis. The ribosomal protein lateral stalk subunit P0 (RPLP0) has recently gathered widespread attention as a crucial factor in the pathological progression of various neoplasms; however, its exact role in HCC remains inadequately defined. Consequently, the present study endeavored to shed light on the function and mechanistic underpinnings of RPLP0 in HCC and assess its clinical significance and potential as a therapeutic target. qPCR and western blot analyses indicated that RPLP0 was markedly upregulated in HCC, with its elevated levels correlating with poorer survival outcomes. Silencing RPLP0 expression suppre

SUBMITTER: Meng Y 

PROVIDER: S-EPMC12674198 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature