DCAF7 Acts as A Scaffold to Recruit USP10 for G3BP1 Deubiquitylation and Facilitates Chemoresistance and Metastasis in Nasopharyngeal Carcinoma
Despite docetaxel combined with cisplatin and 5‐fluorouracil (TPF) being the established treatment for advanced nasopharyngeal carcinoma (NPC), there are patients who do not respond positively to this form of therapy. However, the mechanisms underlying this lack of benefit remain unclear. DCAF7 is i...
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| Published in | Advanced science Vol. 11; no. 36; pp. e2403262 - n/a |
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| Main Authors | , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
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Germany
John Wiley & Sons, Inc
01.09.2024
John Wiley and Sons Inc Wiley |
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| Abstract | Despite docetaxel combined with cisplatin and 5‐fluorouracil (TPF) being the established treatment for advanced nasopharyngeal carcinoma (NPC), there are patients who do not respond positively to this form of therapy. However, the mechanisms underlying this lack of benefit remain unclear. DCAF7 is identified as a chemoresistance gene attenuating the response to TPF therapy in NPC patients. DCAF7 promotes the cisplatin resistance and metastasis of NPC cells in vitro and in vivo. Mechanistically, DCAF7 serves as a scaffold protein that facilitates the interaction between USP10 and G3BP1, leading to the elimination of K48‐linked ubiquitin moieties from Lys76 of G3BP1. This process helps prevent the degradation of G3BP1 via the ubiquitin‒proteasome pathway and promotes the formation of stress granule (SG)‐like structures. Moreover, knockdown of G3BP1 successfully reversed the formation of SG‐like structures and the oncogenic effects of DCAF7. Significantly, NPC patients with increased levels of DCAF7 showed a high risk of metastasis, and elevated DCAF7 levels are linked to an unfavorable prognosis. The study reveals DCAF7 as a crucial gene for cisplatin resistance and offers further understanding of how chemoresistance develops in NPC. The DCAF7‐USP10‐G3BP1 axis contains potential targets and biomarkers for NPC treatment. |
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| AbstractList | Despite docetaxel combined with cisplatin and 5‐fluorouracil (TPF) being the established treatment for advanced nasopharyngeal carcinoma (NPC), there are patients who do not respond positively to this form of therapy. However, the mechanisms underlying this lack of benefit remain unclear. DCAF7 is identified as a chemoresistance gene attenuating the response to TPF therapy in NPC patients. DCAF7 promotes the cisplatin resistance and metastasis of NPC cells in vitro and in vivo. Mechanistically, DCAF7 serves as a scaffold protein that facilitates the interaction between USP10 and G3BP1, leading to the elimination of K48‐linked ubiquitin moieties from Lys76 of G3BP1. This process helps prevent the degradation of G3BP1 via the ubiquitin‒proteasome pathway and promotes the formation of stress granule (SG)‐like structures. Moreover, knockdown of G3BP1 successfully reversed the formation of SG‐like structures and the oncogenic effects of DCAF7. Significantly, NPC patients with increased levels of DCAF7 showed a high risk of metastasis, and elevated DCAF7 levels are linked to an unfavorable prognosis. The study reveals DCAF7 as a crucial gene for cisplatin resistance and offers further understanding of how chemoresistance develops in NPC. The DCAF7‐USP10‐G3BP1 axis contains potential targets and biomarkers for NPC treatment. Abstract Despite docetaxel combined with cisplatin and 5‐fluorouracil (TPF) being the established treatment for advanced nasopharyngeal carcinoma (NPC), there are patients who do not respond positively to this form of therapy. However, the mechanisms underlying this lack of benefit remain unclear. DCAF7 is identified as a chemoresistance gene attenuating the response to TPF therapy in NPC patients. DCAF7 promotes the cisplatin resistance and metastasis of NPC cells in vitro and in vivo. Mechanistically, DCAF7 serves as a scaffold protein that facilitates the interaction between USP10 and G3BP1, leading to the elimination of K48‐linked ubiquitin moieties from Lys76 of G3BP1. This process helps prevent the degradation of G3BP1 via the ubiquitin‒proteasome pathway and promotes the formation of stress granule (SG)‐like structures. Moreover, knockdown of G3BP1 successfully reversed the formation of SG‐like structures and the oncogenic effects of DCAF7. Significantly, NPC patients with increased levels of DCAF7 showed a high risk of metastasis, and elevated DCAF7 levels are linked to an unfavorable prognosis. The study reveals DCAF7 as a crucial gene for cisplatin resistance and offers further understanding of how chemoresistance develops in NPC. The DCAF7‐USP10‐G3BP1 axis contains potential targets and biomarkers for NPC treatment. Despite docetaxel combined with cisplatin and 5-fluorouracil (TPF) being the established treatment for advanced nasopharyngeal carcinoma (NPC), there are patients who do not respond positively to this form of therapy. However, the mechanisms underlying this lack of benefit remain unclear. DCAF7 is identified as a chemoresistance gene attenuating the response to TPF therapy in NPC patients. DCAF7 promotes the cisplatin resistance and metastasis of NPC cells in vitro and in vivo. Mechanistically, DCAF7 serves as a scaffold protein that facilitates the interaction between USP10 and G3BP1, leading to the elimination of K48-linked ubiquitin moieties from Lys76 of G3BP1. This process helps prevent the degradation of G3BP1 via the ubiquitin‒proteasome pathway and promotes the formation of stress granule (SG)-like structures. Moreover, knockdown of G3BP1 successfully reversed the formation of SG-like structures and the oncogenic effects of DCAF7. Significantly, NPC patients with increased levels of DCAF7 showed a high risk of metastasis, and elevated DCAF7 levels are linked to an unfavorable prognosis. The study reveals DCAF7 as a crucial gene for cisplatin resistance and offers further understanding of how chemoresistance develops in NPC. The DCAF7-USP10-G3BP1 axis contains potential targets and biomarkers for NPC treatment.Despite docetaxel combined with cisplatin and 5-fluorouracil (TPF) being the established treatment for advanced nasopharyngeal carcinoma (NPC), there are patients who do not respond positively to this form of therapy. However, the mechanisms underlying this lack of benefit remain unclear. DCAF7 is identified as a chemoresistance gene attenuating the response to TPF therapy in NPC patients. DCAF7 promotes the cisplatin resistance and metastasis of NPC cells in vitro and in vivo. Mechanistically, DCAF7 serves as a scaffold protein that facilitates the interaction between USP10 and G3BP1, leading to the elimination of K48-linked ubiquitin moieties from Lys76 of G3BP1. This process helps prevent the degradation of G3BP1 via the ubiquitin‒proteasome pathway and promotes the formation of stress granule (SG)-like structures. Moreover, knockdown of G3BP1 successfully reversed the formation of SG-like structures and the oncogenic effects of DCAF7. Significantly, NPC patients with increased levels of DCAF7 showed a high risk of metastasis, and elevated DCAF7 levels are linked to an unfavorable prognosis. The study reveals DCAF7 as a crucial gene for cisplatin resistance and offers further understanding of how chemoresistance develops in NPC. The DCAF7-USP10-G3BP1 axis contains potential targets and biomarkers for NPC treatment. Despite docetaxel combined with cisplatin and 5‐fluorouracil (TPF) being the established treatment for advanced nasopharyngeal carcinoma (NPC), there are patients who do not respond positively to this form of therapy. However, the mechanisms underlying this lack of benefit remain unclear. DCAF7 is identified as a chemoresistance gene attenuating the response to TPF therapy in NPC patients. DCAF7 promotes the cisplatin resistance and metastasis of NPC cells in vitro and in vivo. Mechanistically, DCAF7 serves as a scaffold protein that facilitates the interaction between USP10 and G3BP1, leading to the elimination of K48‐linked ubiquitin moieties from Lys76 of G3BP1. This process helps prevent the degradation of G3BP1 via the ubiquitin‒proteasome pathway and promotes the formation of stress granule (SG)‐like structures. Moreover, knockdown of G3BP1 successfully reversed the formation of SG‐like structures and the oncogenic effects of DCAF7. Significantly, NPC patients with increased levels of DCAF7 showed a high risk of metastasis, and elevated DCAF7 levels are linked to an unfavorable prognosis. The study reveals DCAF7 as a crucial gene for cisplatin resistance and offers further understanding of how chemoresistance develops in NPC. The DCAF7‐USP10‐G3BP1 axis contains potential targets and biomarkers for NPC treatment. DCAF7 is identified as a key chemoresistance gene enhancing cisplatin resistance and metastasis in NPC, serving as a scaffold that recruits USP10 to eliminate K48‐linked ubiquitin moieties from Lys76 of G3BP1, thus promoting the formation of stress granule‐like structures. High levels of DCAF7 correlate with metastasis risk and poor prognosis, providing potential targets for overcoming NPC chemoresistance. |
| Author | Li, Qing‐Jie Tang, Ling‐Long Li, Ying‐Qin He, Shi‐Wei Zhao, Yin Li, Jun‐Yan Huang, Cheng‐Long Huang, Sheng‐Yan Liu, Na Lin, Jia‐Yi Ma, Jun Gong, Sha Fang, Xue‐Liang |
| AuthorAffiliation | 1 Sun Yat‐sen University Cancer Center State Key Laboratory of Oncology in South China Collaborative Innovation Center of Cancer Medicine Guangdong Key Laboratory of Nasopharyngeal Carcinoma Diagnosis and Therapy 651 Dongfeng Road East Guangzhou Guangdong 510060 China |
| AuthorAffiliation_xml | – name: 1 Sun Yat‐sen University Cancer Center State Key Laboratory of Oncology in South China Collaborative Innovation Center of Cancer Medicine Guangdong Key Laboratory of Nasopharyngeal Carcinoma Diagnosis and Therapy 651 Dongfeng Road East Guangzhou Guangdong 510060 China |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/38973296$$D View this record in MEDLINE/PubMed |
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| Copyright | 2024 The Author(s). Advanced Science published by Wiley‐VCH GmbH. 2024. This work is published under http://creativecommons.org/licenses/by/4.0/ (the "License"). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. 2024 The Author(s). Advanced Science published by Wiley‐VCH GmbH |
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| Keywords | chemoresistance nasopharyngeal carcinoma chemotherapy DCAF7 deubiquitylation |
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| Snippet | Despite docetaxel combined with cisplatin and 5‐fluorouracil (TPF) being the established treatment for advanced nasopharyngeal carcinoma (NPC), there are... Despite docetaxel combined with cisplatin and 5-fluorouracil (TPF) being the established treatment for advanced nasopharyngeal carcinoma (NPC), there are... Abstract Despite docetaxel combined with cisplatin and 5‐fluorouracil (TPF) being the established treatment for advanced nasopharyngeal carcinoma (NPC), there... |
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| SubjectTerms | Alzheimer's disease Animals Apoptosis Cancer Cell adhesion & migration Cell cycle Cell growth Cell Line, Tumor chemoresistance Chemotherapy Cisplatin - pharmacology DCAF7 deubiquitylation Disease Models, Animal DNA Helicases - genetics DNA Helicases - metabolism Drug Resistance, Neoplasm - genetics Humans Medical prognosis Metastasis Mice nasopharyngeal carcinoma Nasopharyngeal Carcinoma - drug therapy Nasopharyngeal Carcinoma - genetics Nasopharyngeal Carcinoma - metabolism Nasopharyngeal Carcinoma - pathology Nasopharyngeal Neoplasms - drug therapy Nasopharyngeal Neoplasms - genetics Nasopharyngeal Neoplasms - metabolism Nasopharyngeal Neoplasms - pathology Neoplasm Metastasis - genetics Poly-ADP-Ribose Binding Proteins - genetics Poly-ADP-Ribose Binding Proteins - metabolism Proteins RNA Helicases - genetics RNA Helicases - metabolism RNA Recognition Motif Proteins - genetics RNA Recognition Motif Proteins - metabolism Tumors Ubiquitin Thiolesterase - genetics Ubiquitin Thiolesterase - metabolism Ubiquitination - genetics |
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| Title | DCAF7 Acts as A Scaffold to Recruit USP10 for G3BP1 Deubiquitylation and Facilitates Chemoresistance and Metastasis in Nasopharyngeal Carcinoma |
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