USP11 induce resistance to 5-Fluorouracil in Colorectal Cancer through activating autophagy by stabilizing VCP

Chemotherapy plays an important role in the treatment of patients with colorectal cancer (CRC). However, the resistance to chemotherapy severely affects the prognosis of CRC patients and the mechanisms are still poorly understood. Our study investigated the role of ubiquitin-specific protease 11 (US...

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Autores principales: Sun, Hongze, Wang, Rangrang, Liu, Yuan, Mei, Haitao, Liu, Xueni, Peng, Zhihai
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Ivyspring International Publisher 2021
Materias:
Research Paper
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7974880/
https://www.ncbi.nlm.nih.gov/pubmed/33758608
http://dx.doi.org/10.7150/jca.52158
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author Sun, Hongze
Wang, Rangrang
Liu, Yuan
Mei, Haitao
Liu, Xueni
Peng, Zhihai
author_facet Sun, Hongze
Wang, Rangrang
Liu, Yuan
Mei, Haitao
Liu, Xueni
Peng, Zhihai
author_sort Sun, Hongze
collection PubMed
description Chemotherapy plays an important role in the treatment of patients with colorectal cancer (CRC). However, the resistance to chemotherapy severely affects the prognosis of CRC patients and the mechanisms are still poorly understood. Our study investigated the role of ubiquitin-specific protease 11 (USP11) in CRC chemotherapy and found that USP11 could induce resistance to 5-fluorouracil by activating autophagy. A series of in vitro and in vivo experiments revealed that USP11 promoted autophagy through AMPK/Akt/mTOR pathway via stabilizing valosin-containing protein (VCP). Overall, our study demonstrated that USP11 might be valuable to predict the chemotherapeutic sensitivity and improve the prognosis of CRC patients.
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spelling pubmed-79748802021-03-22 USP11 induce resistance to 5-Fluorouracil in Colorectal Cancer through activating autophagy by stabilizing VCP Sun, Hongze Wang, Rangrang Liu, Yuan Mei, Haitao Liu, Xueni Peng, Zhihai J Cancer Research Paper Chemotherapy plays an important role in the treatment of patients with colorectal cancer (CRC). However, the resistance to chemotherapy severely affects the prognosis of CRC patients and the mechanisms are still poorly understood. Our study investigated the role of ubiquitin-specific protease 11 (USP11) in CRC chemotherapy and found that USP11 could induce resistance to 5-fluorouracil by activating autophagy. A series of in vitro and in vivo experiments revealed that USP11 promoted autophagy through AMPK/Akt/mTOR pathway via stabilizing valosin-containing protein (VCP). Overall, our study demonstrated that USP11 might be valuable to predict the chemotherapeutic sensitivity and improve the prognosis of CRC patients. Ivyspring International Publisher 2021-02-22 /pmc/articles/PMC7974880/ /pubmed/33758608 http://dx.doi.org/10.7150/jca.52158 Text en © The author(s) This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions.
spellingShingle Research Paper
Sun, Hongze
Wang, Rangrang
Liu, Yuan
Mei, Haitao
Liu, Xueni
Peng, Zhihai
USP11 induce resistance to 5-Fluorouracil in Colorectal Cancer through activating autophagy by stabilizing VCP
title USP11 induce resistance to 5-Fluorouracil in Colorectal Cancer through activating autophagy by stabilizing VCP
title_full USP11 induce resistance to 5-Fluorouracil in Colorectal Cancer through activating autophagy by stabilizing VCP
title_fullStr USP11 induce resistance to 5-Fluorouracil in Colorectal Cancer through activating autophagy by stabilizing VCP
title_full_unstemmed USP11 induce resistance to 5-Fluorouracil in Colorectal Cancer through activating autophagy by stabilizing VCP
title_short USP11 induce resistance to 5-Fluorouracil in Colorectal Cancer through activating autophagy by stabilizing VCP
title_sort usp11 induce resistance to 5-fluorouracil in colorectal cancer through activating autophagy by stabilizing vcp
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7974880/
https://www.ncbi.nlm.nih.gov/pubmed/33758608
http://dx.doi.org/10.7150/jca.52158
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