The deubiquitinating enzyme USP1 modulates ERα and modulates breast cancer progression

Niu, Zhiguo; Li, Xin; Feng, Suyin; Huang, Qingsong; Zhuang, Ting; Yan, CH; Qian, Hui; Ding, Youming; Zhu, Jian; Xu, Wei

doi:10.7150/jca.50477

Cited by 21 publications

(19 citation statements)

References 27 publications

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“…As a key component of UPS, DUBs participate in the regulation of cell cycle, apoptosis, proliferation and other behaviors [ 25 ]. Importantly, the dysregulation of DUBs leads to the progression of numerous human malignancies, including digestive cancers [ 26 ], breast cancer [ 27 – 29 ], OSCC [ 30 ] and HNSCC [ 31 ]. In this study, we analyzed public databases online and identified several significantly upregulated DUBs including JOSD1.…”

Section: Discussionmentioning

confidence: 99%

JOSD1 promotes proliferation and chemoresistance of head and neck squamous cell carcinoma under the epigenetic regulation of BRD4

et al. 2021

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Background Deubiquitinating enzymes (DUBs) play critical roles in various cancers by modulating functional proteins post-translationally. Previous studies have demonstrated that DUB Josephin Domain Containing 1 (JOSD1) is implicated in tumor progression, however, the role and mechanism of JOSD1 in head and neck squamous cell carcinoma (HNSCC) remain to be explored. In this study, we aimed to identify the clinical significance and function of JOSD1 in HNSCC. Methods The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases were analyzed to find novel DUBs in HNSCC. Immunohistochemistry assay was performed to determine the expression of JOSD1 in our cohort of 42 patients suffered with HNSCC. Kaplan–Meier analysis was used to identify the correlation between JOSD1 and the prognosis of HNSCC patients. The regulation of BRD4 on JOSD1 was determined by using pharmacological inhibition and gene depletion. The in vitro and in vivo experiments were conducted to elucidate the role of JOSD1 in HNSCC. Results The results of IHC showed that JOSD1 was aberrantly expressed in HNSCC specimens, especially in the chemoresistant ones. The overexpression of JOSD1 indicated poor clinical outcome of HNSCC patients. Moreover, JOSD1 depletion dramatically impaired cell proliferation and colony formation, and promoted cisplatin-induced apoptosis of HNSCC cells in vitro. Additionally, JOSD1 suppression inhibited the tumor growth and improved chemosensitivity in vivo. The epigenetic regulator BRD4 contributed to the upregulation of JOSD1 in HNSCC. Conclusions These results demonstrate that JOSD1 functions as an oncogene in HNSCC progression, and provide a promising target for clinical diagnosis and therapy of HNSCC.

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Section: Discussionmentioning

confidence: 99%

JOSD1 promotes proliferation and chemoresistance of head and neck squamous cell carcinoma under the epigenetic regulation of BRD4

et al. 2021

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“…Several DUBs, such as USP1, USP7, and USP22, have been shown to play regulatory roles in ERα signaling. They deubiquitinate ERα and activate its relative signaling pathway to promote ERα + breast cancer development [ 76 , 77 , 78 ]. USP11 positively regulates ERα transcriptional activity in breast cancer cells in an E2-dependent manner [ 79 ].…”

Section: Breast Cancermentioning

confidence: 99%

Deubiquitinases in Cancers: Aspects of Proliferation, Metastasis, and Apoptosis

Liu

LEUNG

Liang

et al. 2022

Cancers

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Deubiquitinases (DUBs) deconjugate ubiquitin (UBQ) from ubiquitylated substrates to regulate its activity and stability. They are involved in several cellular functions. In addition to the general biological regulation of normal cells, studies have demonstrated their critical roles in various cancers. In this review, we evaluated and grouped the biological roles of DUBs, including proliferation, metastasis, and apoptosis, in the most common cancers in the world (liver, breast, prostate, colorectal, pancreatic, and lung cancers). The current findings in these cancers are summarized, and the relevant mechanisms and relationship between DUBs and cancers are discussed. In addition to highlighting the importance of DUBs in cancer biology, this study also provides updated information on the roles of DUBs in different types of cancers.

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“…USP1 is also an essential deubiquitinase in ERα signaling, which enhances ERα stability through cleaving its Lys48-linked ubiquitin chains. According to TCGA and KMPLOT databases, high expression of USP1 is relevant to poor prognosis in ERα + breast cancer patients [ 93 ].…”

Section: Dubs In Chemoresistance and Chemosensitivity Of Breast Cancermentioning

confidence: 99%

Roles and Mechanisms of Deubiquitinases (DUBs) in Breast Cancer Progression and Targeted Drug Discovery

Zhang

Wei

2021

Life

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Deubiquitinase (DUB) is an essential component in the ubiquitin—proteasome system (UPS) by removing ubiquitin chains from substrates, thus modulating the expression, activity, and localization of many proteins that contribute to tumor development and progression. DUBs have emerged as promising prognostic indicators and drug targets. DUBs have shown significant roles in regulating breast cancer growth, metastasis, resistance to current therapies, and several canonical oncogenic signaling pathways. In addition, specific DUB inhibitors have been identified and are expected to benefit breast cancer patients in the future. Here, we review current knowledge about the effects and molecular mechanisms of DUBs in breast cancer, providing novel insight into treatments of breast cancer-targeting DUBs.

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The deubiquitinating enzyme USP1 modulates ERα and modulates breast cancer progression

Cited by 21 publications

References 27 publications

JOSD1 promotes proliferation and chemoresistance of head and neck squamous cell carcinoma under the epigenetic regulation of BRD4

JOSD1 promotes proliferation and chemoresistance of head and neck squamous cell carcinoma under the epigenetic regulation of BRD4

Deubiquitinases in Cancers: Aspects of Proliferation, Metastasis, and Apoptosis

Roles and Mechanisms of Deubiquitinases (DUBs) in Breast Cancer Progression and Targeted Drug Discovery

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