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FBXO22, an epigenetic multiplayer coordinating senescence, hormone signaling, and metastasis
Ubiquitin‐dependent protein degradation has been implicated in the control of various cellular processes such as cell cycle control, transcriptional regulation, DNA damage repair, and apoptosis, many of which are involved in the initiation, progression, metastasis, and drug resistance of cancers. E3...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7419058/ https://www.ncbi.nlm.nih.gov/pubmed/32536008 http://dx.doi.org/10.1111/cas.14534 |
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author | Johmura, Yoshikazu Harris, Alexander S. Ohta, Tomohiko Nakanishi, Makoto |
author_facet | Johmura, Yoshikazu Harris, Alexander S. Ohta, Tomohiko Nakanishi, Makoto |
author_sort | Johmura, Yoshikazu |
collection | PubMed |
description | Ubiquitin‐dependent protein degradation has been implicated in the control of various cellular processes such as cell cycle control, transcriptional regulation, DNA damage repair, and apoptosis, many of which are involved in the initiation, progression, metastasis, and drug resistance of cancers. E3 ubiquitin ligases are known to be the second most prevalent cancer‐related functional gene family next to protein kinases. Of these, FBXO22, an F‐box receptor subunit of SCF E3 ligase, has recently been proposed to play a critical role in multiple aspects related to cancer development and therapy response. Firstly, FBXO22 is a key regulator of senescence induction through ubiquitylation of p53 for degradation. FBXO22 also acts as a molecular switch for the antagonistic and agonistic actions of selective estrogen receptor modulators (SERM) and determines the sensitivity of breast cancer to SERM by ubiquitylating KDM4B complexed with unliganded or SERMs‐bound estrogen receptor (ER). Furthermore, FBXO22 binds to Bach1, a pro‐metastatic transcription factor, suppressing Bach1‐driven metastasis of lung adenocarcinoma, and loss of FBXO22 facilitates metastasis. These findings, as well as other reports, unveiled strikingly important roles of FBXO22 in cancer development and therapeutic strategy. In this review, we summarize recent findings of how FBXO22 regulates major cancer suppression pathways. |
format | Online Article Text |
id | pubmed-7419058 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-74190582020-08-12 FBXO22, an epigenetic multiplayer coordinating senescence, hormone signaling, and metastasis Johmura, Yoshikazu Harris, Alexander S. Ohta, Tomohiko Nakanishi, Makoto Cancer Sci Review Articles Ubiquitin‐dependent protein degradation has been implicated in the control of various cellular processes such as cell cycle control, transcriptional regulation, DNA damage repair, and apoptosis, many of which are involved in the initiation, progression, metastasis, and drug resistance of cancers. E3 ubiquitin ligases are known to be the second most prevalent cancer‐related functional gene family next to protein kinases. Of these, FBXO22, an F‐box receptor subunit of SCF E3 ligase, has recently been proposed to play a critical role in multiple aspects related to cancer development and therapy response. Firstly, FBXO22 is a key regulator of senescence induction through ubiquitylation of p53 for degradation. FBXO22 also acts as a molecular switch for the antagonistic and agonistic actions of selective estrogen receptor modulators (SERM) and determines the sensitivity of breast cancer to SERM by ubiquitylating KDM4B complexed with unliganded or SERMs‐bound estrogen receptor (ER). Furthermore, FBXO22 binds to Bach1, a pro‐metastatic transcription factor, suppressing Bach1‐driven metastasis of lung adenocarcinoma, and loss of FBXO22 facilitates metastasis. These findings, as well as other reports, unveiled strikingly important roles of FBXO22 in cancer development and therapeutic strategy. In this review, we summarize recent findings of how FBXO22 regulates major cancer suppression pathways. John Wiley and Sons Inc. 2020-07-17 2020-08 /pmc/articles/PMC7419058/ /pubmed/32536008 http://dx.doi.org/10.1111/cas.14534 Text en © 2020 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association. This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes. |
spellingShingle | Review Articles Johmura, Yoshikazu Harris, Alexander S. Ohta, Tomohiko Nakanishi, Makoto FBXO22, an epigenetic multiplayer coordinating senescence, hormone signaling, and metastasis |
title | FBXO22, an epigenetic multiplayer coordinating senescence, hormone signaling, and metastasis |
title_full | FBXO22, an epigenetic multiplayer coordinating senescence, hormone signaling, and metastasis |
title_fullStr | FBXO22, an epigenetic multiplayer coordinating senescence, hormone signaling, and metastasis |
title_full_unstemmed | FBXO22, an epigenetic multiplayer coordinating senescence, hormone signaling, and metastasis |
title_short | FBXO22, an epigenetic multiplayer coordinating senescence, hormone signaling, and metastasis |
title_sort | fbxo22, an epigenetic multiplayer coordinating senescence, hormone signaling, and metastasis |
topic | Review Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7419058/ https://www.ncbi.nlm.nih.gov/pubmed/32536008 http://dx.doi.org/10.1111/cas.14534 |
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