A patent review of the ubiquitin ligase system: 2015–2018

Li, Xin; Ekinci, Elmira; Rohondia, Sagar; Wang, Jicang; Liu, Jinbao; Dou, Q. Ping

doi:10.1080/13543776.2018.1549229

Cited by 65 publications

(41 citation statements)

References 140 publications

(173 reference statements)

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“…β-TrCP is an E3 ubiquitin ligase that regulates the expression of a variety of proteins 19 . YAP is phosphorylated by Hippo/LATS signaling kinase, causing YAP to remain in the cytoplasm 20 .…”

Section: Resultsmentioning

confidence: 99%

Aspirin attenuates YAP and β-catenin expression by promoting β-TrCP to overcome docetaxel and vinorelbine resistance in triple-negative breast cancer

Fan

Tang

et al. 2020

Cell Death Dis

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The use of aspirin has been associated with reduced breast cancer risk, but it is litter known if aspirin overcomes chemoresistance in triple-negative breast cancer (TNBC). Herein, we demonstrated that changes in the expression of Yes-associated protein (YAP) and β-catenin might be a promising predictive biomarker for neoadjuvant chemotherapy sensitivity in TNBC patients. Inhibition of YAP or β-catenin enhanced the cytotoxicity of the anti-microtubule agents docetaxel and vinorelbine against drug-resistant TNBC cells as well as the sensitivity of these cells to the agents in vitro and in vivo. Interestingly, aspirin not only significantly inhibited the growth of TNBC cells, but also attenuated YAP and β-catenin expression by upregulating the E3 ubiquitin ligase β-TrCP to abolished docetaxel and vinorelbine resistance. The combination of aspirin and docetaxel or vinorelbine remarkably inhibited the growth of drug-resistant TNBC cells in vitro and in vivo. Moreover, TNBC patients with high YAP and/or β-catenin expression had a higher risk of relapse or mortality than patients with low YAP and/or β-catenin expression. Collectively, our study discovered a novel role of aspirin based on its anticancer effect, and put forward some possible mechanisms of chemoresistance in TNBC. The combined use of aspirin and anti-microtubule drugs presented several promising therapeutic approaches for TNBC treatment.

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Section: Resultsmentioning

confidence: 99%

Aspirin attenuates YAP and β-catenin expression by promoting β-TrCP to overcome docetaxel and vinorelbine resistance in triple-negative breast cancer

Fan

Tang

et al. 2020

Cell Death Dis

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“…Our results demonstrated that HPV E7 promoted the ubiquitin-proteasome-mediated degradation of IFI16. The ubiquitin-proteasome system is mainly composed of ubiquitin-activating enzyme (E1), ubiquitin-crosslinking enzyme (E2), ubiquitin ligase (E3) and the 26S proteasome [32]. Among these components, the E3 ubiquitin ligase is responsible for target protein recognition and mediates the degradation of substrates by the 26S proteasome [33].…”

Section: Hpv E7 Interacts With Ifi16 and E3 Ligasetrim21mentioning

confidence: 99%

HPV E7 inhibits cell pyroptosis by promoting TRIM21-mediated degradation and ubiquitination of the IFI16 inflammasome

Song¹,

Wu²,

Xu³

et al. 2020

Int. J. Biol. Sci.

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Human papillomavirus (HPV) is a DNA virus that causes sexually transmitted infections. The HPV oncoprotein E7 plays a critical role in the regulation of host immunity to promote the immune escape of HPV and the occurrence of cervical cancer or genital warts. Pyroptosis, a highly inflammatory form of programmed cell death, can be induced by inflammasomes and acts as a defense against pathogenic infection. However, whether HPV E7 can regulate cell pyroptosis to evade immune surveillance has not been determined. In this study, we found that HPV E7 could inhibit cell pyroptosis induced by transfection with dsDNA. The activation of the inflammasome, and the production of IL-18 and IL-1β were also restrained by HPV E7. Mass spectrometry and immunoprecipitation showed that HPV E7 interacted with IFI16 and TRIM21. We also discovered that HPV E7 recruited the E3 ligase TRIM21 to ubiquitinate and degrade the IFI16 inflammasome, leading to the inhibition of cell pyroptosis and self-escape from immune surveillance. Thus, our study reveals an important immune escape mechanism in HPV infection and may provide targets for the development of a novel immunotherapeutic strategy to effectively restore antiviral immunity.

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“…Some authors consider U-box (UFD2 homology) as a third subfamily. U-box ubiquitin-ligases act as scaffold proteins that recruit the ubiquitin-charged E2 enzyme and the substrate protein to docking sites [ 54 , 55 ]. Moreover, another novel family that shares features of RING and HECT is named RING-between-RING ligases (RBR).…”

Section: Molecular Mechanisms Of Emt In Cancer: Role Of Targeted Pmentioning

confidence: 99%

Regulation of Epithelial–Mesenchymal Plasticity by the E3 Ubiquitin-Ligases in Cancer

Rodríguez-Alonso

Casas-Pais

Roca-Lema

et al. 2020

Cancers

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The epithelial–mesenchymal plasticity (EMP) is a process by which epithelial cells acquire the ability to dynamically switch between epithelial and mesenchymal phenotypic cellular states. Epithelial cell plasticity in the context of an epithelial-to-mesenchymal transition (EMT) confers increased cell motility, invasiveness and the ability to disseminate to distant sites and form metastasis. The modulation of molecularly defined targets involved in this process has become an attractive therapeutic strategy against cancer. Protein degradation carried out by ubiquitination has gained attention as it can selectively degrade proteins of interest. In the ubiquitination reaction, the E3 ubiquitin-ligases are responsible for the specific binding of ubiquitin to a small subset of target proteins, and are considered promising anticancer drug targets. In this review, we summarize the role of the E3 ubiquitin-ligases that control targeted protein degradation in cancer-EMT, and we highlight the potential use of the E3 ubiquitin-ligases as drug targets for the development of small-molecule drugs against cancer.

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A patent review of the ubiquitin ligase system: 2015–2018

Cited by 65 publications

References 140 publications

Aspirin attenuates YAP and β-catenin expression by promoting β-TrCP to overcome docetaxel and vinorelbine resistance in triple-negative breast cancer

Aspirin attenuates YAP and β-catenin expression by promoting β-TrCP to overcome docetaxel and vinorelbine resistance in triple-negative breast cancer

HPV E7 inhibits cell pyroptosis by promoting TRIM21-mediated degradation and ubiquitination of the IFI16 inflammasome

Regulation of Epithelial–Mesenchymal Plasticity by the E3 Ubiquitin-Ligases in Cancer

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