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Identification of autophagy‐related genes signature predicts chemotherapeutic and immunotherapeutic efficiency in bladder cancer (BLCA)

Autophagy maintains cellular homeostasis by degrading and recycling cytoplasmic components under stress conditions, which is identified to be involved in tumorigenesis and now has been recognized as novel target in cancer treatment. In present study, we gathered total autophagy‐related genes and est...

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Autores principales: Cao, Rui, Ma, Bo, Wang, Gang, Xiong, Yaoyi, Tian, Ye, Yuan, Lushun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8184684/
https://www.ncbi.nlm.nih.gov/pubmed/33960661
http://dx.doi.org/10.1111/jcmm.16552
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author Cao, Rui
Ma, Bo
Wang, Gang
Xiong, Yaoyi
Tian, Ye
Yuan, Lushun
author_facet Cao, Rui
Ma, Bo
Wang, Gang
Xiong, Yaoyi
Tian, Ye
Yuan, Lushun
author_sort Cao, Rui
collection PubMed
description Autophagy maintains cellular homeostasis by degrading and recycling cytoplasmic components under stress conditions, which is identified to be involved in tumorigenesis and now has been recognized as novel target in cancer treatment. In present study, we gathered total autophagy‐related genes and established an autophagy‐related genes signature (ATGRS) through LASSO cox regression analysis in BLCA. Kaplan‐Meier survival and multivariate cox regression analyses both showed the ATGRS was a robust independent prognostic factor with high accuracy. Subsequently, integrated analyses indicated that ATGRS had a strong correlation with molecular subtypes, clinicopathological characteristics and somatic mutation alteration. Moreover, ATGRS was found to be positively correlated with the infiltration of immune cells in tumour microenvironment (TME) and immune checkpoint expression, indicating the potent role of autophagy by regulating the TME. In addition, ATGRS was proved to be efficient in predicting the clinical benefit of immune checkpoint inhibitors (ICIs) based immunotherapy and chemotherapy in BLCA. Furthermore, we observed abnormal expression levels of autophagy‐related genes and found the different behaviour of ATGRS in pancancer by LASSO cox regression analysis. Therefore, construction of ATGRS in BLCA could help us to interpret the underlying mechanism of autophagy and sheds a light on the clinical application for a combination of autophagy modification with targeted immunotherapy and chemotherapy in BLCA.
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spelling pubmed-81846842021-06-15 Identification of autophagy‐related genes signature predicts chemotherapeutic and immunotherapeutic efficiency in bladder cancer (BLCA) Cao, Rui Ma, Bo Wang, Gang Xiong, Yaoyi Tian, Ye Yuan, Lushun J Cell Mol Med Original Articles Autophagy maintains cellular homeostasis by degrading and recycling cytoplasmic components under stress conditions, which is identified to be involved in tumorigenesis and now has been recognized as novel target in cancer treatment. In present study, we gathered total autophagy‐related genes and established an autophagy‐related genes signature (ATGRS) through LASSO cox regression analysis in BLCA. Kaplan‐Meier survival and multivariate cox regression analyses both showed the ATGRS was a robust independent prognostic factor with high accuracy. Subsequently, integrated analyses indicated that ATGRS had a strong correlation with molecular subtypes, clinicopathological characteristics and somatic mutation alteration. Moreover, ATGRS was found to be positively correlated with the infiltration of immune cells in tumour microenvironment (TME) and immune checkpoint expression, indicating the potent role of autophagy by regulating the TME. In addition, ATGRS was proved to be efficient in predicting the clinical benefit of immune checkpoint inhibitors (ICIs) based immunotherapy and chemotherapy in BLCA. Furthermore, we observed abnormal expression levels of autophagy‐related genes and found the different behaviour of ATGRS in pancancer by LASSO cox regression analysis. Therefore, construction of ATGRS in BLCA could help us to interpret the underlying mechanism of autophagy and sheds a light on the clinical application for a combination of autophagy modification with targeted immunotherapy and chemotherapy in BLCA. John Wiley and Sons Inc. 2021-05-07 2021-06 /pmc/articles/PMC8184684/ /pubmed/33960661 http://dx.doi.org/10.1111/jcmm.16552 Text en © 2021 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd. 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
Cao, Rui
Ma, Bo
Wang, Gang
Xiong, Yaoyi
Tian, Ye
Yuan, Lushun
Identification of autophagy‐related genes signature predicts chemotherapeutic and immunotherapeutic efficiency in bladder cancer (BLCA)
title Identification of autophagy‐related genes signature predicts chemotherapeutic and immunotherapeutic efficiency in bladder cancer (BLCA)
title_full Identification of autophagy‐related genes signature predicts chemotherapeutic and immunotherapeutic efficiency in bladder cancer (BLCA)
title_fullStr Identification of autophagy‐related genes signature predicts chemotherapeutic and immunotherapeutic efficiency in bladder cancer (BLCA)
title_full_unstemmed Identification of autophagy‐related genes signature predicts chemotherapeutic and immunotherapeutic efficiency in bladder cancer (BLCA)
title_short Identification of autophagy‐related genes signature predicts chemotherapeutic and immunotherapeutic efficiency in bladder cancer (BLCA)
title_sort identification of autophagy‐related genes signature predicts chemotherapeutic and immunotherapeutic efficiency in bladder cancer (blca)
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8184684/
https://www.ncbi.nlm.nih.gov/pubmed/33960661
http://dx.doi.org/10.1111/jcmm.16552
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