New relationship of E2F1 and BNIP3 with caveolin‐1 in lung cancer‐associated fibroblasts

In recent years, studies have found that E2F1, a downstream effector of caveolin‐1 (Cav‐1), participates in tumor cell metabolic reprogramming. E2F1 modulates mitochondrial fusion and mitophagy. Bioinformatic analysis has identified the E2F1‐MFN2 axis as a regulator of mitophagy. Our data establish...

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Autores principales: Shen, Cheng, Chen, Xuanming, Xiao, Kai, Che, Guowei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley & Sons Australia, Ltd 2020
Materias:
Commentaries
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7262894/
https://www.ncbi.nlm.nih.gov/pubmed/32212370
http://dx.doi.org/10.1111/1759-7714.13408
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author Shen, Cheng
Chen, Xuanming
Xiao, Kai
Che, Guowei
author_facet Shen, Cheng
Chen, Xuanming
Xiao, Kai
Che, Guowei
author_sort Shen, Cheng
collection PubMed
description In recent years, studies have found that E2F1, a downstream effector of caveolin‐1 (Cav‐1), participates in tumor cell metabolic reprogramming. E2F1 modulates mitochondrial fusion and mitophagy. Bioinformatic analysis has identified the E2F1‐MFN2 axis as a regulator of mitophagy. Our data establish a new novel paradigm for regulation of the tumor cell metabolic reprogramming pathway by Cav‐1 that is operationally linked and mutually dependent on the transcriptional activation of E2F1 and induces mitophagy with BNIP3 in cancer‐associated fibroblasts (CAFs).
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spelling pubmed-72628942020-06-01 New relationship of E2F1 and BNIP3 with caveolin‐1 in lung cancer‐associated fibroblasts Shen, Cheng Chen, Xuanming Xiao, Kai Che, Guowei Thorac Cancer Commentaries In recent years, studies have found that E2F1, a downstream effector of caveolin‐1 (Cav‐1), participates in tumor cell metabolic reprogramming. E2F1 modulates mitochondrial fusion and mitophagy. Bioinformatic analysis has identified the E2F1‐MFN2 axis as a regulator of mitophagy. Our data establish a new novel paradigm for regulation of the tumor cell metabolic reprogramming pathway by Cav‐1 that is operationally linked and mutually dependent on the transcriptional activation of E2F1 and induces mitophagy with BNIP3 in cancer‐associated fibroblasts (CAFs). John Wiley & Sons Australia, Ltd 2020-03-25 2020-06 /pmc/articles/PMC7262894/ /pubmed/32212370 http://dx.doi.org/10.1111/1759-7714.13408 Text en © 2020 The Authors. Thoracic Cancer published by China Lung Oncology Group and John Wiley & Sons Australia, Ltd This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
spellingShingle Commentaries
Shen, Cheng
Chen, Xuanming
Xiao, Kai
Che, Guowei
New relationship of E2F1 and BNIP3 with caveolin‐1 in lung cancer‐associated fibroblasts
title New relationship of E2F1 and BNIP3 with caveolin‐1 in lung cancer‐associated fibroblasts
title_full New relationship of E2F1 and BNIP3 with caveolin‐1 in lung cancer‐associated fibroblasts
title_fullStr New relationship of E2F1 and BNIP3 with caveolin‐1 in lung cancer‐associated fibroblasts
title_full_unstemmed New relationship of E2F1 and BNIP3 with caveolin‐1 in lung cancer‐associated fibroblasts
title_short New relationship of E2F1 and BNIP3 with caveolin‐1 in lung cancer‐associated fibroblasts
title_sort new relationship of e2f1 and bnip3 with caveolin‐1 in lung cancer‐associated fibroblasts
topic Commentaries
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7262894/
https://www.ncbi.nlm.nih.gov/pubmed/32212370
http://dx.doi.org/10.1111/1759-7714.13408
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