FBXO22, an epigenetic multiplayer coordinating senescence, hormone signaling, and metastasis.,Cancer Science

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FBXO22, an epigenetic multiplayer coordinating senescence, hormone signaling, and metastasis.
Cancer Science ( IF 4.5 ) Pub Date : 2020-06-14 , DOI: 10.1111/cas.14534
Yoshikazu Johmura ₁ , Alexander S Harris ₁ , Tomohiko Ohta ₂ , Makoto Nakanishi ₁

Affiliation

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.

中文翻译：

FBXO22，一种表观遗传的多人游戏，可协调衰老，激素信号传导和转移。

泛素依赖性蛋白降解涉及各种细胞过程的控制，例如细胞周期控制，转录调节，DNA损伤修复和凋亡，其中许多与癌症的发生，进展，转移和耐药有关。E3泛素连接酶是仅次于蛋白激酶的第二大最普遍的癌症相关功能基因家族。其中，最近有人提出，FBXO22是SCF E3连接酶的F-box受体亚基，在与癌症发展和治疗反应有关的多个方面起着关键作用。首先，FBXO22是通过p53泛素化降解来诱导衰老的关键调节因子。FBXO22还可作为选择性雌激素受体调节剂（SERM）拮抗和激动作用的分子开关，并通过泛素化结合有未配体或SERMs结合的雌激素受体（ER）的KDM4B来确定乳腺癌对SERM的敏感性。此外，FBXO22结合前转移转录因子Bach1，抑制Bach1驱动的肺腺癌转移，而FBXO22的丢失则促进了转移。这些发现以及其他报告揭示了FBXO22在癌症发展和治疗策略中的重要作用。在这篇综述中，我们总结了FBXO22如何调节主要的癌症抑制途径的最新发现。转移前转录因子，可抑制Bach1驱动的肺腺癌转移，而FBXO22的丢失则有助于转移。这些发现以及其他报告揭示了FBXO22在癌症发展和治疗策略中的重要作用。在这篇综述中，我们总结了FBXO22如何调节主要的癌症抑制途径的最新发现。转移前转录因子，可抑制Bach1驱动的肺腺癌转移，而FBXO22的丢失则有助于转移。这些发现以及其他报告揭示了FBXO22在癌症发展和治疗策略中的重要作用。在这篇综述中，我们总结了FBXO22如何调节主要的癌症抑制途径的最新发现。

更新日期：2020-08-12

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