FAM60A promotes osteosarcoma development and progression

Abstract 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 databas...

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Main Authors: Yu Sun, Yu‐Nan Man, Jin‐hui Cheng, Jing‐tang Li, Ya‐yun Liu
Format: Article
Language:English
Published: Wiley 2023-08-01
Series:Cancer Medicine
Subjects:
Online Access:https://doi.org/10.1002/cam4.6343
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author Yu Sun
Yu‐Nan Man
Jin‐hui Cheng
Jing‐tang Li
Ya‐yun Liu
author_facet Yu Sun
Yu‐Nan Man
Jin‐hui Cheng
Jing‐tang Li
Ya‐yun Liu
author_sort Yu Sun
collection DOAJ
description Abstract 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.
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spelling doaj.art-746f1253606f444c859c9be0c5d934522024-03-27T09:11:01ZengWileyCancer Medicine2045-76342023-08-011216174911750310.1002/cam4.6343FAM60A promotes osteosarcoma development and progressionYu Sun0Yu‐Nan Man1Jin‐hui Cheng2Jing‐tang Li3Ya‐yun Liu4Division of Spinal Surgery The First Affiliated Hospital of Guangxi Medical University Nanning Guangxi Zhuang Autonomous Region P.R. ChinaDivision of Spinal Surgery The First Affiliated Hospital of Guangxi Medical University Nanning Guangxi Zhuang Autonomous Region P.R. ChinaJiangxi Provincial People's Hospital The First Affiliated Hospital of Nanchang Medical College Nanchang Jiangxi ChinaJiangxi Provincial People's Hospital The First Affiliated Hospital of Nanchang Medical College Nanchang Jiangxi ChinaJiangxi Provincial People's Hospital The First Affiliated Hospital of Nanchang Medical College Nanchang Jiangxi ChinaAbstract 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.https://doi.org/10.1002/cam4.6343clinical significancefamily of homology 60Ahub genesosteosarcoma
spellingShingle Yu Sun
Yu‐Nan Man
Jin‐hui Cheng
Jing‐tang Li
Ya‐yun Liu
FAM60A promotes osteosarcoma development and progression
Cancer Medicine
clinical significance
family of homology 60A
hub genes
osteosarcoma
title FAM60A promotes osteosarcoma development and progression
title_full FAM60A promotes osteosarcoma development and progression
title_fullStr FAM60A promotes osteosarcoma development and progression
title_full_unstemmed FAM60A promotes osteosarcoma development and progression
title_short FAM60A promotes osteosarcoma development and progression
title_sort fam60a promotes osteosarcoma development and progression
topic clinical significance
family of homology 60A
hub genes
osteosarcoma
url https://doi.org/10.1002/cam4.6343
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AT yunanman fam60apromotesosteosarcomadevelopmentandprogression
AT jinhuicheng fam60apromotesosteosarcomadevelopmentandprogression
AT jingtangli fam60apromotesosteosarcomadevelopmentandprogression
AT yayunliu fam60apromotesosteosarcomadevelopmentandprogression