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Association of RDM1 with osteosarcoma progression via cell cycle and MEK/ERK signalling pathway regulation
RAD52 motif‐containing 1 (RDM1), a key regulator of DNA double‐strand break repair and recombination, has been reported to play an important role in the development of various human cancers, such as papillary thyroid carcinoma, neuroblastoma and lung cancer. However, the effect of RDM1 on osteosarco...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8358872/ https://www.ncbi.nlm.nih.gov/pubmed/34264012 http://dx.doi.org/10.1111/jcmm.16735 |
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author | Sheng, Jun Liu, Kun Sun, Dawei Nie, Piming Mu, Zhiping Chen, Hui Zhang, Zhengfeng |
author_facet | Sheng, Jun Liu, Kun Sun, Dawei Nie, Piming Mu, Zhiping Chen, Hui Zhang, Zhengfeng |
author_sort | Sheng, Jun |
collection | PubMed |
description | RAD52 motif‐containing 1 (RDM1), a key regulator of DNA double‐strand break repair and recombination, has been reported to play an important role in the development of various human cancers, such as papillary thyroid carcinoma, neuroblastoma and lung cancer. However, the effect of RDM1 on osteosarcoma (OS) progression remains unclear. Here, this study mainly explored the connection between RDM1 and OS progression, as well as the underlying mechanism. It was found that RDM1 was highly expressed in OS cells compared with human osteoblast cells. Knockdown of RDM1 caused OS cell proliferation inhibition, cell apoptosis promotion and cell cycle arrest at G1 stage, whereas RDM1 overexpression resulted in the opposite phenotypes. Furthermore, RDM1 silencing leads to a significant decrease in tumour growth in xenograft mouse model. RDM1 also increased the protein levels of MEK 1/2 and ERK 1/2. All these findings suggest that RDM1 plays an oncogenic role in OS via stimulating cell cycle transition from G1 to S stage, and regulating MEK/ERK signalling pathway, providing a promising therapeutic factor for the treatment of OS. |
format | Online Article Text |
id | pubmed-8358872 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-83588722021-08-15 Association of RDM1 with osteosarcoma progression via cell cycle and MEK/ERK signalling pathway regulation Sheng, Jun Liu, Kun Sun, Dawei Nie, Piming Mu, Zhiping Chen, Hui Zhang, Zhengfeng J Cell Mol Med Original Articles RAD52 motif‐containing 1 (RDM1), a key regulator of DNA double‐strand break repair and recombination, has been reported to play an important role in the development of various human cancers, such as papillary thyroid carcinoma, neuroblastoma and lung cancer. However, the effect of RDM1 on osteosarcoma (OS) progression remains unclear. Here, this study mainly explored the connection between RDM1 and OS progression, as well as the underlying mechanism. It was found that RDM1 was highly expressed in OS cells compared with human osteoblast cells. Knockdown of RDM1 caused OS cell proliferation inhibition, cell apoptosis promotion and cell cycle arrest at G1 stage, whereas RDM1 overexpression resulted in the opposite phenotypes. Furthermore, RDM1 silencing leads to a significant decrease in tumour growth in xenograft mouse model. RDM1 also increased the protein levels of MEK 1/2 and ERK 1/2. All these findings suggest that RDM1 plays an oncogenic role in OS via stimulating cell cycle transition from G1 to S stage, and regulating MEK/ERK signalling pathway, providing a promising therapeutic factor for the treatment of OS. John Wiley and Sons Inc. 2021-07-15 2021-08 /pmc/articles/PMC8358872/ /pubmed/34264012 http://dx.doi.org/10.1111/jcmm.16735 Text en © 2021 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine. 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 | Original Articles Sheng, Jun Liu, Kun Sun, Dawei Nie, Piming Mu, Zhiping Chen, Hui Zhang, Zhengfeng Association of RDM1 with osteosarcoma progression via cell cycle and MEK/ERK signalling pathway regulation |
title | Association of RDM1 with osteosarcoma progression via cell cycle and MEK/ERK signalling pathway regulation |
title_full | Association of RDM1 with osteosarcoma progression via cell cycle and MEK/ERK signalling pathway regulation |
title_fullStr | Association of RDM1 with osteosarcoma progression via cell cycle and MEK/ERK signalling pathway regulation |
title_full_unstemmed | Association of RDM1 with osteosarcoma progression via cell cycle and MEK/ERK signalling pathway regulation |
title_short | Association of RDM1 with osteosarcoma progression via cell cycle and MEK/ERK signalling pathway regulation |
title_sort | association of rdm1 with osteosarcoma progression via cell cycle and mek/erk signalling pathway regulation |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8358872/ https://www.ncbi.nlm.nih.gov/pubmed/34264012 http://dx.doi.org/10.1111/jcmm.16735 |
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