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Chondroitin Polymerizing Factor (CHPF) promotes cell proliferation and tumor growth in human osteosarcoma by inhibiting SKP2's ubiquitination while activating the AKT pathway

Osteosarcoma is a common malignant tumor occurring in children and young adults. Chondroitin sulfate (CS) participates in cell adhesion, cell division, and the formation of neural networks in the body, the biosynthesis of which requires the participation of glycosyltransferases. CHPF, a glycosyltran...

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Autores principales: Shen, Yi, Li, Jun, Peng, Dan, Liao, Lele, Chen, Xia, Zhong, Weiye, Liu, Zicheng, Yu, Chao, Sun, Yuanliang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Chongqing Medical University 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10363583/
https://www.ncbi.nlm.nih.gov/pubmed/37492722
http://dx.doi.org/10.1016/j.gendis.2022.06.010
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author Shen, Yi
Li, Jun
Peng, Dan
Liao, Lele
Chen, Xia
Zhong, Weiye
Liu, Zicheng
Yu, Chao
Sun, Yuanliang
author_facet Shen, Yi
Li, Jun
Peng, Dan
Liao, Lele
Chen, Xia
Zhong, Weiye
Liu, Zicheng
Yu, Chao
Sun, Yuanliang
author_sort Shen, Yi
collection PubMed
description Osteosarcoma is a common malignant tumor occurring in children and young adults. Chondroitin sulfate (CS) participates in cell adhesion, cell division, and the formation of neural networks in the body, the biosynthesis of which requires the participation of glycosyltransferases. CHPF, a glycosyltransferase, plays a role in the extension of CS. Recently, CHPF's biological roles and functional importance in human diseases including malignant tumors have been widely discussed. However, whether CHPF is involved in osteosarcoma development and growth has not been revealed. The present work aimed to investigate the expression levels, functional significance and molecular mechanism of CHPF in osteosarcoma progression. Our results revealed that CHPF is strongly expressed in osteosarcoma tissues and cells. Furthermore, CHPF serves as a tumor promoter in the development and progression of osteosarcoma through enhancing cell proliferation and migration while suppressing apoptosis. Exploration of the mechanism by which CHPF promotes osteosarcoma indicated that CHPF promotes osteosarcoma through counteracting SKP2's ubiquitination and activating the Akt signaling pathway. For the first time, we clarified the roles of CHPF in osteosarcoma, and our results suggested that CHPF might be a novel therapeutic target in the treatment strategies for osteosarcoma.
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spelling pubmed-103635832023-07-25 Chondroitin Polymerizing Factor (CHPF) promotes cell proliferation and tumor growth in human osteosarcoma by inhibiting SKP2's ubiquitination while activating the AKT pathway Shen, Yi Li, Jun Peng, Dan Liao, Lele Chen, Xia Zhong, Weiye Liu, Zicheng Yu, Chao Sun, Yuanliang Genes Dis Full Length Article Osteosarcoma is a common malignant tumor occurring in children and young adults. Chondroitin sulfate (CS) participates in cell adhesion, cell division, and the formation of neural networks in the body, the biosynthesis of which requires the participation of glycosyltransferases. CHPF, a glycosyltransferase, plays a role in the extension of CS. Recently, CHPF's biological roles and functional importance in human diseases including malignant tumors have been widely discussed. However, whether CHPF is involved in osteosarcoma development and growth has not been revealed. The present work aimed to investigate the expression levels, functional significance and molecular mechanism of CHPF in osteosarcoma progression. Our results revealed that CHPF is strongly expressed in osteosarcoma tissues and cells. Furthermore, CHPF serves as a tumor promoter in the development and progression of osteosarcoma through enhancing cell proliferation and migration while suppressing apoptosis. Exploration of the mechanism by which CHPF promotes osteosarcoma indicated that CHPF promotes osteosarcoma through counteracting SKP2's ubiquitination and activating the Akt signaling pathway. For the first time, we clarified the roles of CHPF in osteosarcoma, and our results suggested that CHPF might be a novel therapeutic target in the treatment strategies for osteosarcoma. Chongqing Medical University 2022-08-06 /pmc/articles/PMC10363583/ /pubmed/37492722 http://dx.doi.org/10.1016/j.gendis.2022.06.010 Text en © 2022 The Authors. Publishing services by Elsevier B.V. on behalf of KeAi Communications Co., Ltd. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Full Length Article
Shen, Yi
Li, Jun
Peng, Dan
Liao, Lele
Chen, Xia
Zhong, Weiye
Liu, Zicheng
Yu, Chao
Sun, Yuanliang
Chondroitin Polymerizing Factor (CHPF) promotes cell proliferation and tumor growth in human osteosarcoma by inhibiting SKP2's ubiquitination while activating the AKT pathway
title Chondroitin Polymerizing Factor (CHPF) promotes cell proliferation and tumor growth in human osteosarcoma by inhibiting SKP2's ubiquitination while activating the AKT pathway
title_full Chondroitin Polymerizing Factor (CHPF) promotes cell proliferation and tumor growth in human osteosarcoma by inhibiting SKP2's ubiquitination while activating the AKT pathway
title_fullStr Chondroitin Polymerizing Factor (CHPF) promotes cell proliferation and tumor growth in human osteosarcoma by inhibiting SKP2's ubiquitination while activating the AKT pathway
title_full_unstemmed Chondroitin Polymerizing Factor (CHPF) promotes cell proliferation and tumor growth in human osteosarcoma by inhibiting SKP2's ubiquitination while activating the AKT pathway
title_short Chondroitin Polymerizing Factor (CHPF) promotes cell proliferation and tumor growth in human osteosarcoma by inhibiting SKP2's ubiquitination while activating the AKT pathway
title_sort chondroitin polymerizing factor (chpf) promotes cell proliferation and tumor growth in human osteosarcoma by inhibiting skp2's ubiquitination while activating the akt pathway
topic Full Length Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10363583/
https://www.ncbi.nlm.nih.gov/pubmed/37492722
http://dx.doi.org/10.1016/j.gendis.2022.06.010
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