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miR-559 Inhibits Proliferation, Autophagy, and Angiogenesis of Hepatocellular Carcinoma Cells by Targeting PARD3

Hepatocellular carcinoma (HCC) is one of the most common cancers in the world and has a high mortality rate. Although prevention and treatment of HCC has improved, it still faces poor prognosis and high mortality. miRNAs play a critical role in the tumorigenesis of HCC, but the underlying mechanism...

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Detalles Bibliográficos
Autores principales: Wang, Chunjing, Li, Chengcheng, Hao, Rui
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9467804/
https://www.ncbi.nlm.nih.gov/pubmed/36105681
http://dx.doi.org/10.1155/2022/3121492
Descripción
Sumario:Hepatocellular carcinoma (HCC) is one of the most common cancers in the world and has a high mortality rate. Although prevention and treatment of HCC has improved, it still faces poor prognosis and high mortality. miRNAs play a critical role in the tumorigenesis of HCC, but the underlying mechanism has not been well investigated. Here, the functions and interaction between miR-559 and PARD3 were investigated in HCC cells. Increased PARD3 and decreased miR-559 expression were observed in HCC cells compared with those in normal liver cells, especially in Huh-7 cells. Studies further demonstrated that PARD3 silencing or miR-559 overexpression impaired the proliferation, autophagy, and angiogenesis in Huh-7 cells. Mechanistically, PARD3 represents a target of miR-559. Furthermore, investigations revealed that miR-559 inhibition induced the expression of PARD3, thereby enhancing cell proliferation, autophagy, and angiogenesis in Huh-7 cells. These results reveal the interaction between miR-559 and PARD3 in HCC cells and provide new insights into their potential targets as therapeutic treatment against HCC.