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Cancers
Special Issues
Deubiquitylating Enzymes and Their Contribution to Human Malignancies
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Deubiquitylating Enzymes and Their Contribution to Human Malignancies

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".

Deadline for manuscript submissions: 31 May 2024 | Viewed by 5530

Special Issue Editor

Dr. Tarek Abbas

E-Mail Website
Guest Editor
Department of Radiation Oncology, University of Virginia, 1300 Jefferson Park Avenue, Charlottesville, VA, USA
Interests: genomic instability and human cancer; ubiquitin-dependent regulation of DNA replication; cellular responses to DNA damage; DNA damage repair
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Deubiquitinating enzymes (DUBs), a class of enzymes that remove ubiquitin or ubiquitin-like peptide chains from substrate proteins, play key roles in disease development, including cancer. In addition to mutations in their coding sequences, the expression of several DUBs is dysregulated in a large number of human malignancies, suggesting a significant role for these enzymes in the initiation and/or progression of human cancer, and may additionally modulate the cancer sensitivity to conventional chemotherapy. In fact, recent studies show that dysregulated expression of DUBs plays important roles for the development of drug resistance, thus making this class of enzymes attractive targets for new drug development. Novel insights into the molecular mechanisms through which deregulated DUB expression enables cancer cells to escape cell death mechanisms, survive the tumor microenvironment, and disseminate to distant organs are beginning to emerge.

In this Special Issue of Cancers, we are interested in articles reporting on the identification and/or characterization of DUBs specifically relevant to human malignancy and potentially involved in the regulation of genome maintenance mechanisms, epigenetic control, cell cycle control, DNA damage sensing and repair, and cellular death mechanisms. Primary articles focusing on mechanistic understanding of the role of DUBs in the development of various human cancers or the development of resistance to therapies, as well as the development of new animal models of deregulated DUB activity, are highly encouraged. Articles that describe the development of new methodologies aiming at better screening/identification for novel DUB substrates with a direct link to cancer initiation or progression would be of great interest. Additionally, review articles that summarize current knowledge about the role of DUBs in human cancer and/or the development of new therapeutic modalities targeting DUBs would be particularly useful. Potential topics include but are not limited to:

  • Role of DUBs in cancer initiation and progression;
  • Role of deubiquitinases in cancer therapy and resistance;
  • Novel molecular pathways underlying the role of DUBs in human malignancies;
  • Genetic cancer models of deregulated DUB activity;
  • DUBs and the tumor microenvironment;
  • Methods of screening/identification of cancer-specific DUB targets;
  • Rational design of small molecules with selective inhibitory activity for individual DUBs for cancer therapy;
  • Description and characterization of novel DUB inhibitors for the treatment of cancer or cancer drug resistance.

Dr. Tarek Abbas
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • deubiquitinases
  • DUBs
  • proteolysis in cancer
  • pharmacological DUB inhibitors
  • drug resistance

Published Papers (2 papers)

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Research

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16 pages, 5043 KiB  
Article
UCHL5 Promotes Proliferation and Migration of Bladder Cancer Cells by Activating c-Myc via AKT/mTOR Signaling
by Yuanfei Cao, Xin Yan, Xiaojie Bai, Feng Tang, Penghui Si, Can Bai, Kuerban Tuoheti, Linfa Guo, Zuhaer Yisha, Tao Liu and Tongzu Liu
Cancers 2022, 14(22), 5538; https://doi.org/10.3390/cancers14225538 - 10 Nov 2022
Cited by 6 | Viewed by 1916
Abstract
Ubiquitin C-terminal hydrolase L5 (UCHL5) is a deubiquitinating enzyme (DUB) that removes ubiquitin from its substrates. Associations between UCHL5 and cancer have been reported in various tissues, but the effect of UCHL5 on bladder cancer has not been thoroughly investigated. This study investigates [...] Read more.
Ubiquitin C-terminal hydrolase L5 (UCHL5) is a deubiquitinating enzyme (DUB) that removes ubiquitin from its substrates. Associations between UCHL5 and cancer have been reported in various tissues, but the effect of UCHL5 on bladder cancer has not been thoroughly investigated. This study investigates the expression and function of UCHL5 in bladder cancer. UCHL5 was shown to be abnormally expressed using IHC of tissue microarray and Western blotting. Several procedures were performed to assess the effect of UCHL5 overexpression or knockdown on bladder cancer, such as cell proliferation, colony formation, wound-healing, and Transwell assays. In addition, RNA-Seq and Western blotting experiments were used to verify the status of downstream signaling pathways. Finally, bladder cancers with knockdown or overexpression of UCHL5 were treated with either SC79 or LY294002 to examine the participation of the AKT/mTOR signaling pathway and the expression of downstream targets c-Myc, SLC25A19, and ICAM5. In contrast to adjacent tissue samples, we discovered that UCHL5 was substantially expressed in bladder cancer samples. We also found that UCHL5 downregulation significantly suppressed both tumor growth in vivo and cell proliferation and migration in vitro. According to RNA-Seq analyses and Western blotting experiments, the expression of c-Myc, SLC25A19, and ICAM5 was modified as a result of UCHL5 activating AKT/mTOR signaling in bladder cancer cells. All things considered, our findings show that increased UCHL5 expression stimulates AKT/mTOR signaling, subsequently triggering the expression of c-Myc, SLC25A19, and ICAM5, which in turn promotes carcinogenesis in bladder cancer. UCHL5 is therefore a potential target for therapy in bladder cancer patients. Full article
(This article belongs to the Special Issue Deubiquitylating Enzymes and Their Contribution to Human Malignancies)
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Review

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15 pages, 2464 KiB  
Review
USP7 Inhibitors in Cancer Immunotherapy: Current Status and Perspective
by Georgiy Korenev, Sergey Yakukhnov, Anastasia Druk, Anastasia Golovina, Vitaly Chasov, Regina Mirgayazova, Roman Ivanov and Emil Bulatov
Cancers 2022, 14(22), 5539; https://doi.org/10.3390/cancers14225539 - 10 Nov 2022
Cited by 9 | Viewed by 3116
Abstract
Ubiquitin-specific protease 7 (USP7) regulates the stability of a plethora of intracellular proteins involved in the suppression of anti-tumor immune responses and its overexpression is associated with poor survival in many cancers. USP7 impairs the balance of the p53/MDM2 axis resulting in the [...] Read more.
Ubiquitin-specific protease 7 (USP7) regulates the stability of a plethora of intracellular proteins involved in the suppression of anti-tumor immune responses and its overexpression is associated with poor survival in many cancers. USP7 impairs the balance of the p53/MDM2 axis resulting in the proteasomal degradation of the p53 tumor suppressor, a process that can be reversed by small-molecule inhibitors of USP7. USP7 was shown to regulate the anti-tumor immune responses in several cases. Its inhibition impedes the function of regulatory T cells, promotes polarization of tumor-associated macrophages, and reduces programmed death-ligand 1 (PD-L1) expression in tumor cells. The efficacy of small-molecule USP7 inhibitors was demonstrated in vivo. The synergistic effect of combining USP7 inhibition with cancer immunotherapy is a promising therapeutic approach, though its clinical efficacy is yet to be proven. In this review, we focus on the recent developments in understanding the intrinsic role of USP7, its interplay with other molecular pathways, and the therapeutic potential of targeting USP7 functions. Full article
(This article belongs to the Special Issue Deubiquitylating Enzymes and Their Contribution to Human Malignancies)
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