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PAIP1 is a novel oncogene in human hepatocellular carcinoma

BACKGROUND: Poly(A)-binding protein interacting protein 1 (PAIP1) is a translational initiation regulatory factor that has been reported as oncogene in multiple malignant diseases. However, its role in hepatocellular carcinoma (HCC) and the potential mechanisms have not been explored. METHODS: PAIP1...

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Detalles Bibliográficos
Autores principales: Zhang, Nuobei, Chen, Xin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer US 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9702235/
https://www.ncbi.nlm.nih.gov/pubmed/36436074
http://dx.doi.org/10.1007/s12672-022-00530-0
Descripción
Sumario:BACKGROUND: Poly(A)-binding protein interacting protein 1 (PAIP1) is a translational initiation regulatory factor that has been reported as oncogene in multiple malignant diseases. However, its role in hepatocellular carcinoma (HCC) and the potential mechanisms have not been explored. METHODS: PAIP1 expression level in HCC cell lines were detected by real-time quantitative PCR and western blotting. The proliferation and colony formation of HCC cell lines were detected by MTT and colony formation assay. The apoptosis and cell cycle were detected by flow cytometry. The volume and growth rate of the xenograft tumors were observed. The potential mechanism of PAIP1 was analyzed by miRNA Microarray Analysis and TargetScan analysis. RESULTS: PAIP1 is significantly upregulated in HCC cell lines. PAIP1 knockdown dramatically inhibits cell proliferation and colony formation, induces apoptosis and alters the cell cycle distribution by increasing the G2/M cell percentage. Moreover, PAIP1 knockdown significantly reduces tumorigenesis in a murine transplantation model. Bioinformatics and immunoblotting analysis reveal that PAIP1 knockdown dysregulates cyclin D pathway-related proteins. CONCLUSION: PAIP1 plays an oncogenic role in hepatocellular carcinoma. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s12672-022-00530-0.