PNO1 regulates autophagy and apoptosis of hepatocellular carcinoma via the MAPK signaling pathway

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作者
Zhiqiang Han
Dongming Liu
Lu Chen
Yuchao He
Xiangdong Tian
Lisha Qi
Liwei Chen
Yi Luo
Ziye Chen
Xiaomeng Hu
Guangtao Li
Linlin Zhan
Yu Wang
Qiang Li
Peng Chen
Zhiyong Liu
Hua Guo
机构
[1] Tianjin Medical University Cancer Institute and Hospital,Department of Tumor Cell Biology
[2] Tianjin Medical University Cancer Institute and Hospital,Department of Hepatobiliary Cancer, Liver Cancer Research Center
[3] Tianjin’s Clinical Research Center for Cancer,Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy
[4] Tianjin Medical University Cancer Institute and Hospital,Department of Endoscopy
[5] Tianjin Medical University Cancer Institute and Hospital,Department of Pathology
[6] Tianjin Medical University Cancer Institute and Hospital,Department of Thoracic Oncology, Lung Cancer Diagnosis and Treatment Center
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摘要
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.
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