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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...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2023
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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 |
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author | Sun, Yu Man, Yu‐Nan Cheng, Jin‐hui Li, Jing‐tang Liu, Ya‐yun |
author_facet | Sun, Yu Man, Yu‐Nan Cheng, Jin‐hui Li, Jing‐tang Liu, Ya‐yun |
author_sort | Sun, Yu |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-10501228 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-105012282023-09-15 FAM60A promotes osteosarcoma development and progression Sun, Yu Man, Yu‐Nan Cheng, Jin‐hui Li, Jing‐tang Liu, Ya‐yun Cancer Med Research Articles 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. John Wiley and Sons Inc. 2023-07-12 /pmc/articles/PMC10501228/ /pubmed/37439040 http://dx.doi.org/10.1002/cam4.6343 Text en © 2023 The Authors. Cancer Medicine published by John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Articles Sun, Yu Man, Yu‐Nan Cheng, Jin‐hui Li, Jing‐tang Liu, Ya‐yun FAM60A promotes osteosarcoma development and progression |
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 | Research Articles |
url | 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 |
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