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Chondroitin polymerizing factor (CHPF) promotes development of malignant melanoma through regulation of CDK1
Chondroitin polymerizing factor (CHPF) is an important member of glycosyltransferases involved in the biosynthesis of chondroitin sulfate (CS). However, the relationship between CHPF and malignant melanoma (MM) is still unknown. In this study, it was demonstrated that CHPF was up-regulated in MM tis...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7329816/ https://www.ncbi.nlm.nih.gov/pubmed/32612115 http://dx.doi.org/10.1038/s41419-020-2526-9 |
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author | Sun, Wei Zhao, Fang Xu, Yu Huang, Kai Guo, Xianling Zheng, Biqiang Liu, Xin Luo, Zhiguo Kong, Yunyi Xu, Midie Schadendorf, Dirk Chen, Yong |
author_facet | Sun, Wei Zhao, Fang Xu, Yu Huang, Kai Guo, Xianling Zheng, Biqiang Liu, Xin Luo, Zhiguo Kong, Yunyi Xu, Midie Schadendorf, Dirk Chen, Yong |
author_sort | Sun, Wei |
collection | PubMed |
description | Chondroitin polymerizing factor (CHPF) is an important member of glycosyltransferases involved in the biosynthesis of chondroitin sulfate (CS). However, the relationship between CHPF and malignant melanoma (MM) is still unknown. In this study, it was demonstrated that CHPF was up-regulated in MM tissues compared with the adjacent normal skin tissues and its high expression was correlated with more advanced T stage. Further investigations indicated that the over-expression/knockdown of CHPF could promote/inhibit proliferation, colony formation and migration of MM cells, while inhibiting/promoting cell apoptosis. Moreover, knockdown of CHPF could also suppress tumorigenicity of MM cells in vivo. RNA-sequencing followed by Ingenuity pathway analysis (IPA) was performed for exploring downstream of CHPF and identified CDK1 as the potential target. Furthermore, our study revealed that knockdown of CDK1 could inhibit development of MM in vitro, and alleviate the CHPF over-expression induced promotion of MM. In conclusion, our study showed, as the first time, CHPF as a tumor promotor for MM, whose function was carried out probably through the regulation of CDK1. |
format | Online Article Text |
id | pubmed-7329816 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-73298162020-07-06 Chondroitin polymerizing factor (CHPF) promotes development of malignant melanoma through regulation of CDK1 Sun, Wei Zhao, Fang Xu, Yu Huang, Kai Guo, Xianling Zheng, Biqiang Liu, Xin Luo, Zhiguo Kong, Yunyi Xu, Midie Schadendorf, Dirk Chen, Yong Cell Death Dis Article Chondroitin polymerizing factor (CHPF) is an important member of glycosyltransferases involved in the biosynthesis of chondroitin sulfate (CS). However, the relationship between CHPF and malignant melanoma (MM) is still unknown. In this study, it was demonstrated that CHPF was up-regulated in MM tissues compared with the adjacent normal skin tissues and its high expression was correlated with more advanced T stage. Further investigations indicated that the over-expression/knockdown of CHPF could promote/inhibit proliferation, colony formation and migration of MM cells, while inhibiting/promoting cell apoptosis. Moreover, knockdown of CHPF could also suppress tumorigenicity of MM cells in vivo. RNA-sequencing followed by Ingenuity pathway analysis (IPA) was performed for exploring downstream of CHPF and identified CDK1 as the potential target. Furthermore, our study revealed that knockdown of CDK1 could inhibit development of MM in vitro, and alleviate the CHPF over-expression induced promotion of MM. In conclusion, our study showed, as the first time, CHPF as a tumor promotor for MM, whose function was carried out probably through the regulation of CDK1. Nature Publishing Group UK 2020-07-01 /pmc/articles/PMC7329816/ /pubmed/32612115 http://dx.doi.org/10.1038/s41419-020-2526-9 Text en © The Author(s) 2020 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Sun, Wei Zhao, Fang Xu, Yu Huang, Kai Guo, Xianling Zheng, Biqiang Liu, Xin Luo, Zhiguo Kong, Yunyi Xu, Midie Schadendorf, Dirk Chen, Yong Chondroitin polymerizing factor (CHPF) promotes development of malignant melanoma through regulation of CDK1 |
title | Chondroitin polymerizing factor (CHPF) promotes development of malignant melanoma through regulation of CDK1 |
title_full | Chondroitin polymerizing factor (CHPF) promotes development of malignant melanoma through regulation of CDK1 |
title_fullStr | Chondroitin polymerizing factor (CHPF) promotes development of malignant melanoma through regulation of CDK1 |
title_full_unstemmed | Chondroitin polymerizing factor (CHPF) promotes development of malignant melanoma through regulation of CDK1 |
title_short | Chondroitin polymerizing factor (CHPF) promotes development of malignant melanoma through regulation of CDK1 |
title_sort | chondroitin polymerizing factor (chpf) promotes development of malignant melanoma through regulation of cdk1 |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7329816/ https://www.ncbi.nlm.nih.gov/pubmed/32612115 http://dx.doi.org/10.1038/s41419-020-2526-9 |
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