Abstract
Some studies have reported that activated ribosomes are positively associated with malignant tumors, especially in hepatocellular carcinoma (HCC). The RNA-binding protein PNO1 is a critical ribosome rarely reported in human tumors. This study aimed to explore the molecular mechanisms of PNO1 in HCC. Using 150 formalin-fixed and paraffin-embedded samples and 8 fresh samples, we found high PNO1 expression in HCC tumor tissues through Western blotting and RT-PCR. Moreover, the higher PNO1 expression was associated with poor HCC prognosis patients. In vitro and in vivo experiments indicated that PNO1 overexpression promoted the proliferation and depressed the apoptosis of HCC cells. High PNO1 expression also increased the autophagy of HCC cells. The molecular mechanisms underlying PNO1 were examined by RNA-seq analysis and a series of functional experiments. Results showed that PNO1 promoted HCC progression through the MAPK signaling pathway. Therefore, PNO1 was overexpressed in HCC, promoted autophagy, and inhibited the apoptosis of HCC cells through the MAPK signaling pathway.
Highlights
Hepatocellular carcinoma (HCC) is the fourth most common cause of cancer-related mortality worldwide[1]
We demonstrated that partner of NOB1” (PNO1) was overexpressed in HCC tissues and may act as a specific prognostic biomarker of HCC
PNO1 was overexpressed in HCC tissues and associated with poor prognosis of HCC patients
Summary
Hepatocellular carcinoma (HCC) is the fourth most common cause of cancer-related mortality worldwide[1]. More than 380,000 people die of liver cancer in China each year, accounting for 51% of the global HCC-affected population[2]. Novel molecules should be explored to improve HCC prognosis. One of the cancer hallmarks, is a biological process of energy dependence, cellular autonomy, and orderliness[7,8]. Caspases are ubiquitously expressed cysteine proteases that play a central role in apoptosis[9]. Death-inducing stimuli lead to cleavage at the aspartic residues of caspases and removal of the N-terminal inhibitory domain, resulting in the demolition phase of apoptosis[10,11]. Apoptosis is the main and most well-studied form of programmed cell death
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