USP7 promotes hepatoblastoma progression through activation of PI3K/AKT signaling pathway

Autor:	Rui Dong, Mujie Ye, Jiajun He, Lu-Lu Xie, Duan Ma, Baihui Liu, Xiangqi Liu, Meng Wei, Kuiran Dong, Jingjing Zhang, Kai Li
Rok vydání:	2021
Předmět:	Hepatoblastoma Male Cancer Research Down-Regulation Ubiquitin-Specific Peptidase 7 03 medical and health sciences Phosphatidylinositol 3-Kinases 0302 clinical medicine Downregulation and upregulation Genetics medicine Humans PI3K/AKT/mTOR pathway 030304 developmental biology Cell Proliferation 0303 health sciences Akt/PKB signaling pathway Chemistry Cell migration General Medicine Cell cycle medicine.disease Prognosis Oncology Apoptosis 030220 oncology & carcinogenesis Cancer research Disease Progression Female Signal transduction Proto-Oncogene Proteins c-akt Signal Transduction
Zdroj:	Cancer biomarkers : section A of Disease markers. 31(2)
ISSN:	1875-8592
Popis:	BACKGROUND: Hepatoblastoma (HB) is an embryonic solid tumor and the most common primary malignant liver tumor in children. HB usually occurs in infants and children. Although treatment diversity is increasing, some patients still have very poor prognosis. Many studies have investigated USP7 inhibitors for tumors. Using database information, we found that USP7 is highly expressed in HB. METHODS: Lentivirus-mediated USP7 knockdown and overexpression was performed in HB cell lines HepG2 and Huh6. CCK8 and transwell assays were used to determine cell viability and metastasis. Flow cytometry was used to study cell cycle and apoptosis. Levels of proteins were detected using western blots. RESULTS: Downregulation of USP7 resulted in significant decrease in cell proliferation, clonal formation, and cell migration and invasion. With overexpression of USP7, cellular malignant behavior increased. Cell cycle assays showed that USP7 knockdown inhibited G1 to S phase transition in the cell cycle. Upregulation of USP7 promoted the transition. Animal experiments showed USP7 facilitated tumor growth in vivo. Western blots indicated that USP7 may affect HB tumorigenesis through the PI3K/AKT signaling pathway. Furthermore, USP7 inhibitor P5091 inhibited HB development and PI3K/AKT pathway. CONCLUSION: USP7 upregulation contributed to HB genesis and development through the PI3K/AKT signaling pathway. USP7 could be a potential target for future HB treatment.
Databáze:	OpenAIRE
Externí odkaz:	https://explore.openaire.eu/search/publication?articleId=doi_dedup___::821ce7197c0d6e740b052a796328cb95 https://pubmed.ncbi.nlm.nih.gov/33780361 Zobrazit plný text záznamu Plný text ve formátu PDF Plný text ve formátu HTML
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