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FAM60A promotes osteosarcoma development and progression

BACKGROUND: Osteosarcoma (OS) is a highly malignant primary bone tumor. Family of homology 60A (FAM60A) reportedly contributes to the malignant growth of some tumors. METHODS: Herein we investigated the mRNA expression level of FAM60A by combining OS and non‐cancer samples from public databases. Imm...

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Detalles Bibliográficos
Autores principales: Sun, Yu, Man, Yu‐Nan, Cheng, Jin‐hui, Li, Jing‐tang, Liu, Ya‐yun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10501228/
https://www.ncbi.nlm.nih.gov/pubmed/37439040
http://dx.doi.org/10.1002/cam4.6343
Descripción
Sumario:BACKGROUND: Osteosarcoma (OS) is a highly malignant primary bone tumor. Family of homology 60A (FAM60A) reportedly contributes to the malignant growth of some tumors. METHODS: Herein we investigated the mRNA expression level of FAM60A by combining OS and non‐cancer samples from public databases. Immunohistochemistry was performed to determine protein expression levels of FAM60A in patients with OS. Further, RT‐qPCR and western blotting were conducted to evaluate FAM60A expression in various OS cell lines. CCK‐8 assay, colony formation assay, and flow cytometry were applied to determine the function of FAM60A. Finally, functional enrichment analysis was performed based on FAM60A co‐expressed genes. RESULTS: FAM60A mRNA expression level was found to be significantly upregulated (standardized mean difference = 1.27, 95% CI [0.67–1.88]). Survival analyses suggested that higher expression of FAM60A was indicative of poor prognoses. Similarly, FAM60A protein expression level was also observed to be upregulated. Knocking down FAM60A expression inhibited OS cell proliferation, increased apoptosis, and blocked cells from entering the S phase. Besides, cell cycle was the most prominently enriched pathway, and BUB1, DTL, and EXO1 were identified as hub genes. CONCLUSIONS: FAM60A expression was found to be markedly upregulated in OS; furthermore, FAM60A was observed to promote OS cell proliferation, inhibit apoptosis, and participate in cell cycle regulation. Besides, FAM60A may interact with hub genes to participate in the progress of OS.