Deubiquitinating enzyme USP33 restrains docetaxel-induced apoptosis via stabilising the phosphatase DUSP1 in prostate cancer

Guo, Fei; Zhang, Chao; Wang, Fubo; Zhang, Wei; Shi, Xiaolei; Zhu, Yasheng; Fang, Ziyu; Yang, Bo; Sun, Yinghao

doi:10.1038/s41418-019-0473-8

Cited by 41 publications

(26 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Results signify that co-administration of docetaxel and GRP78-siRNA to PC-3 cells elicits enhanced sensitivity of cancer cells to docetaxel both in vitro and in vivo, which might be a result of cell cycle arrest, apoptosis, and autophagy mediated by GRP78 knockdown [62]. Similar to this, knockdown of deubiquitinating enzyme ubiquitin-specific protease 33 (USP33), which is overexpressed in PCa cells, with siRNA considerably induces apoptosis mediated by docetaxel in CRPC [63]. In addition, siRNA-mediated knockdown of USP9X notably decreases anchorage-independent growth of prostate carcinoma cells, possibly through increasing ubiquitination and decreasing protein levels of IGFR (insulin-like growth factor receptor) and IRS-2 (insulin receptor substrate-2), indicating the importance of targeting certain ubiquitin-specific proteases in PCa treatment [64].…”

Section: Attenuating Drug Resistance In Prostate Cancer Using Sirnamentioning

confidence: 60%

Advances in Targeting Cancer-Associated Genes by Designed siRNA in Prostate Cancer

Bahreyni

Luo

2020

Cancers

View full text Add to dashboard Cite

Short interfering RNAs (siRNAs) have provided novel insights into the field of cancer treatment in light of their ability to specifically target and silence cancer-associated genes. In recent years, numerous studies focus on determining genes that actively participate in tumor formation, invasion, and metastasis in order to establish new targets for cancer treatment. In spite of great advances in designing various siRNAs with diverse targets, efficient delivery of siRNAs to cancer cells is still the main challenge in siRNA-mediated cancer treatment. Recent advancements in the field of nanotechnology and nanomedicine hold great promise to meet this challenge. This review focuses on recent findings in cancer-associated genes and the application of siRNAs to successfully silence them in prostate cancer, as well as recent progress for effectual delivery of siRNAs to cancer cells.

show abstract

Section: Attenuating Drug Resistance In Prostate Cancer Using Sirnamentioning

confidence: 60%

Advances in Targeting Cancer-Associated Genes by Designed siRNA in Prostate Cancer

Bahreyni

Luo

2020

Cancers

View full text Add to dashboard Cite

show abstract

“…DUSP1 is reduced in various cancers, including liver cancer, pancreatic cancer, and lung cancer and this gene is considered a tumor suppressor that belongs to the MKP phosphatase family. DUSP1 plays an important role in regulating cell proliferation, tumorigenesis, and drug resistance [37][38][39] . Our findings indicated that EZH2 was able to bind directly to the promoter regions of DUSP1 and induce H3K27 trimethylation.…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA CASC9 promotes gefitinib resistance in NSCLC by epigenetic repression of DUSP1

Chen

Cheng

et al. 2020

Cell Death Dis

View full text Add to dashboard Cite

Resistance to epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs), such as gefitinib, has greatly affected clinical outcomes in non-small cell lung cancer (NSCLC) patients. The long noncoding RNAs (lncRNAs) are known to regulate tumorigenesis and cancer progression, but their contributions to NSCLC gefitinib resistance remain poorly understood. In this study, by analyzing the differentially expressed lncRNAs in gefitinib-resistant cells and gefitinib-sensitive cells in the National Institute of Health GEO dataset, we found that lncRNA CASC9 expression was upregulated, and this was also verified in resistant tissues. Gain and loss of function studies showed that CASC9 inhibition restored gefitinib sensitivity both in vitro and in vivo, whereas CASC9 overexpression promoted gefitinib resistance. Mechanistically, CASC9 repressed the tumor suppressor DUSP1 by recruiting histone methyltransferase EZH2, thereby increasing the resistance to gefitinib. Furthermore, ectopic expression of DUSP1 increased gefitinib sensitivity by inactivating the ERK pathway. Our results highlight the essential role of CASC9 in gefitinib resistance, suggesting that the CASC9/EZH2/DUSP1 axis might be a novel target for overcoming EGFR-TKI resistance in NSCLC.

show abstract

“…Research on DUBs that can regulate CSCs and ITAIMs has great potential for the use of synergistic immunotherapy. The therapeutic effects of DUB inhibitors such as USP1, USP4, USP7, USP14 and USP33 have been confirmed in prostate cancer, lung cancer, breast cancer and hematological malignancies (Ma et al, 2019;Xia et al, 2019a;Guo et al, 2020;Gutierrez-Diaz et al, 2020;Lai et al, 2020).…”

Section: Dubs Involved In Stem Cell Factors Srss and Itaimmentioning

confidence: 98%

Deubiquitinating Enzymes Orchestrate the Cancer Stem Cell-Immunosuppressive Niche Dialogue: New Perspectives and Therapeutic Potential

Guo

Xia

Deng

et al. 2021

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

Cancer stem cells (CSCs) are sparks for igniting tumor recurrence and the instigators of low response to immunotherapy and drug resistance. As one of the important components of tumor microenvironment, the tumor associated immune microenvironment (TAIM) is driving force for the heterogeneity, plasticity and evolution of CSCs. CSCs create the inhibitory TAIM (ITAIM) mainly through four stemness-related signals (SRSs), including Notch-nuclear factor-κB axis, Hedgehog, Wnt and signal transducer and activator of transcription. Ubiquitination and deubiquitination in proteins related to the specific stemness of the CSCs have a profound impact on the regulation of ITAIM. In regulating the balance between ubiquitination and deubiquitination, it is crucial for deubiquitinating enzymes (DUBs) to cleave ubiquitin chains from substrates. Ubiquitin-specific peptidases (USPs) comprise the largest family of DUBs. Growing evidence suggests that they play novel functions in contribution of ITAIM, including regulating tumor immunogenicity, activating stem cell factors, upregulating the SRSs, stabilizing anti-inflammatory receptors, and regulating anti-inflammatory cytokines. These overactive or abnormal signaling may dampen antitumor immune responses. The inhibition of USPs could play a regulatory role in SRSs and reversing ITAIM, and also have great potential in improving immune killing ability against tumor cells, including CSCs. In this review, we focus on the USPs involved in CSCs signaling pathways and regulating ITAIM, which are promising therapeutic targets in antitumor therapy.

show abstract

Deubiquitinating enzyme USP33 restrains docetaxel-induced apoptosis via stabilising the phosphatase DUSP1 in prostate cancer

Cited by 41 publications

References 41 publications

Advances in Targeting Cancer-Associated Genes by Designed siRNA in Prostate Cancer

Advances in Targeting Cancer-Associated Genes by Designed siRNA in Prostate Cancer

Long non-coding RNA CASC9 promotes gefitinib resistance in NSCLC by epigenetic repression of DUSP1

Deubiquitinating Enzymes Orchestrate the Cancer Stem Cell-Immunosuppressive Niche Dialogue: New Perspectives and Therapeutic Potential

Contact Info

Product

Resources

About