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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...

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Autores principales: Johmura, Yoshikazu, Harris, Alexander S., Ohta, Tomohiko, Nakanishi, Makoto
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2020
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.
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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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