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Pleiotropic Pro-tumor Activities Regulated by Overexpressed Yin Yang 1 (YY1)...
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Pleiotropic Pro-tumor Activities Regulated by Overexpressed Yin Yang 1 (YY1) in Human Cancers: Clinical Implications

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

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 6957

Special Issue Editor

Prof. Dr. Benjamin Bonavida

E-Mail Website
Guest Editor
Department of Microbiology, Immunology & Molecular Genetics, David Geffen School of Medicine at UCLA, Jonsson Comprehensive Cancer Center, University of California at Los Angeles, Los Angeles, CA 90095, USA
Interests: cancer biology; immunotherapy; chemotherapy; resistance; RKIP; YY1; NO; metastasis; suppressors; cytotoxicity
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Yin Yang 1 (YY1) is a member of the GLI–Krüppel family of proteins and is a DNA-binding protein with multiple functional domains. YY1 expression is ubiquitous in many normal tissues and diseases. It exhibits many cellular functions. Most human cancers overexpress YY1 and YY1 acts as an oncogene. YY1 modulates many genes that regulate the development and progression of cancer. Among other impacts, it may modulate transcription (as an activator or as a repressor); promote cell viability, cell proliferation, metastasis, drug and immune resistance and metastasis; and inhibit apoptosis and DNA repair. Hence, the inhibition of YY1 results in the reversal of the cancer phenotype and sensitivity of the resistant cancer cells to conventional cytotoxic therapies. In addition to the role of YY1 in both diagnosis and prognosis, practically targeting YY1 specifically in cancer cells, if possible, offers a unique strategy in the treatment of various cancers that is of significant benefit clinically.

For this Special Issue, we welcome original research articles or review papers to address the clinical and therapeutic implications of YY1 in various human cancer types.

Prof. Dr. Benjamin Bonavida
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

  • Yin Yang 1
  • YY1
  • transcriptional regulation
  • overexpression
  • therapeutic potential
  • tumor growth
  • selective targeting
  • tumor phenotype
  • resistance

Published Papers (5 papers)

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Research

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28 pages, 9851 KiB  
Article
Cross-Talks between RKIP and YY1 through a Multilevel Bioinformatics Pan-Cancer Analysis
by Stavroula Baritaki and Apostolos Zaravinos
Cancers 2023, 15(20), 4932; https://doi.org/10.3390/cancers15204932 - 11 Oct 2023
Viewed by 1042
Abstract
Recent studies suggest that PEBP1 (also known as RKIP) and YY1, despite having distinct molecular functions, may interact and mutually influence each other’s activity. They exhibit reciprocal control over each other’s expression through regulatory loops, prompting the hypothesis that their interplay could be [...] Read more.
Recent studies suggest that PEBP1 (also known as RKIP) and YY1, despite having distinct molecular functions, may interact and mutually influence each other’s activity. They exhibit reciprocal control over each other’s expression through regulatory loops, prompting the hypothesis that their interplay could be pivotal in cancer advancement and resistance to drugs. To delve into this interplay’s functional characteristics, we conducted a comprehensive analysis using bioinformatics tools across a range of cancers. Our results confirm the association between elevated YY1 mRNA levels and varying survival outcomes in diverse tumors. Furthermore, we observed differing degrees of inhibitory or activating effects of these two genes in apoptosis, cell cycle, DNA damage, and other cancer pathways, along with correlations between their mRNA expression and immune infiltration. Additionally, YY1/PEBP1 expression and methylation displayed connections with genomic alterations across different cancer types. Notably, we uncovered links between the two genes and different indicators of immunosuppression, such as immune checkpoint blockade response and T-cell dysfunction/exclusion levels, across different patient groups. Overall, our findings underscore the significant role of the interplay between YY1 and PEBP1 in cancer progression, influencing genomic changes, tumor immunity, or the tumor microenvironment. Additionally, these two gene products appear to impact the sensitivity of anticancer drugs, opening new avenues for cancer therapy. Full article
(This article belongs to the Special Issue Pleiotropic Pro-tumor Activities Regulated by Overexpressed Yin Yang 1 (YY1) in Human Cancers: Clinical Implications)
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Review

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15 pages, 1779 KiB  
Review
Clinical Potential of YY1-Hypoxia Axis for Vascular Normalization and to Improve Immunotherapy
by Concetta Meo and Filomena de Nigris
Cancers 2024, 16(3), 491; https://doi.org/10.3390/cancers16030491 - 23 Jan 2024
Viewed by 862
Abstract
Abnormal vasculature in solid tumors causes poor blood perfusion, hypoxia, low pH, and immune evasion. It also shapes the tumor microenvironment and affects response to immunotherapy. The combination of antiangiogenic therapy and immunotherapy has emerged as a promising approach to normalize vasculature and [...] Read more.
Abnormal vasculature in solid tumors causes poor blood perfusion, hypoxia, low pH, and immune evasion. It also shapes the tumor microenvironment and affects response to immunotherapy. The combination of antiangiogenic therapy and immunotherapy has emerged as a promising approach to normalize vasculature and unlock the full potential of immunotherapy. However, the unpredictable and redundant mechanisms of vascularization and immune suppression triggered by tumor-specific hypoxic microenvironments indicate that such combination therapies need to be further evaluated to improve patient outcomes. Here, we provide an overview of the interplay between tumor angiogenesis and immune modulation and review the function and mechanism of the YY1-HIF axis that regulates the vascular and immune tumor microenvironment. Furthermore, we discuss the potential of targeting YY1 and other strategies, such as nanocarrier delivery systems and engineered immune cells (CAR-T), to normalize tumor vascularization and re-establish an immune-permissive microenvironment to enhance the efficacy of cancer therapy. Full article
(This article belongs to the Special Issue Pleiotropic Pro-tumor Activities Regulated by Overexpressed Yin Yang 1 (YY1) in Human Cancers: Clinical Implications)
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27 pages, 5453 KiB  
Review
Zinc Ions Modulate YY1 Activity: Relevance in Carcinogenesis
by Małgorzata Figiel, Adam Kazimierz Górka and Andrzej Górecki
Cancers 2023, 15(17), 4338; https://doi.org/10.3390/cancers15174338 - 30 Aug 2023
Viewed by 1096
Abstract
YY1 is widely recognized as an intrinsically disordered transcription factor that plays a role in development of many cancers. In most cases, its overexpression is correlated with tumor progression and unfavorable patient outcomes. Our latest research focusing on the role of zinc ions [...] Read more.
YY1 is widely recognized as an intrinsically disordered transcription factor that plays a role in development of many cancers. In most cases, its overexpression is correlated with tumor progression and unfavorable patient outcomes. Our latest research focusing on the role of zinc ions in modulating YY1’s interaction with DNA demonstrated that zinc enhances the protein’s multimeric state and affinity to its operator. In light of these findings, changes in protein concentration appear to be just one element relevant to modulating YY1-dependent processes. Thus, alterations in zinc ion concentration can directly and specifically impact the regulation of gene expression by YY1, in line with reports indicating a correlation between zinc ion levels and advancement of certain tumors. This review concentrates on other potential consequences of YY1 interaction with zinc ions that may act by altering charge distribution, conformational state distribution, or oligomerization to influence its interactions with molecular partners that can disrupt gene expression patterns. Full article
(This article belongs to the Special Issue Pleiotropic Pro-tumor Activities Regulated by Overexpressed Yin Yang 1 (YY1) in Human Cancers: Clinical Implications)
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24 pages, 2422 KiB  
Review
Role of YY1 in the Regulation of Anti-Apoptotic Gene Products in Drug-Resistant Cancer Cells
by Megan Jung, Indy Bui and Benjamin Bonavida
Cancers 2023, 15(17), 4267; https://doi.org/10.3390/cancers15174267 - 25 Aug 2023
Cited by 2 | Viewed by 1254
Abstract
Cancer is a leading cause of death among the various diseases encountered in humans. Cancer is not a single entity and consists of numerous different types and subtypes that require various treatment regimens. In the last decade, several milestones in cancer treatments were [...] Read more.
Cancer is a leading cause of death among the various diseases encountered in humans. Cancer is not a single entity and consists of numerous different types and subtypes that require various treatment regimens. In the last decade, several milestones in cancer treatments were accomplished, such as specific targeting agents or revitalizing the dormant anti-tumor immune response. These milestones have resulted in significant positive clinical responses as well as tumor regression and the prolongation of survival in subsets of cancer patients. Hence, in non-responding patients and non-responding relapsed patients, cancers develop intrinsic mechanisms of resistance to cell death via the overexpression of anti-apoptotic gene products. In parallel, the majority of resistant cancers have been reported to overexpress a transcription factor, Yin Yang 1 (YY1), which regulates the chemo-immuno-resistance of cancer cells to therapeutic anticancer cytotoxic agents. The relationship between the overexpression of YY1 and several anti-apoptotic gene products, such as B-cell lymphoma 2 protein (Bcl-2), B-cell lymphoma extra-large (Bcl-xL), myeloid cell leukemia 1 (Mcl-1) and survivin, is investigated in this paper. The findings demonstrate that these anti-apoptotic gene products are regulated, in part, by YY1 at the transcriptional, epigenetic, post-transcriptional and translational levels. While targeting each of the anti-apoptotic gene products individually has been examined and clinically tested for some, this targeting strategy is not effective due to compensation by other overexpressed anti-apoptotic gene products. In contrast, targeting YY1 directly, through small interfering RNAs (siRNAs), gene editing or small molecule inhibitors, can be therapeutically more effective and generalized in YY1-overexpressed resistant cancers. Full article
(This article belongs to the Special Issue Pleiotropic Pro-tumor Activities Regulated by Overexpressed Yin Yang 1 (YY1) in Human Cancers: Clinical Implications)
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31 pages, 2549 KiB  
Review
Targeting Transcription Factor YY1 for Cancer Treatment: Current Strategies and Future Directions
by Rendy Hosea, Sharon Hillary, Shourong Wu and Vivi Kasim
Cancers 2023, 15(13), 3506; https://doi.org/10.3390/cancers15133506 - 05 Jul 2023
Cited by 7 | Viewed by 2165
Abstract
Cancer represents a significant and persistent global health burden, with its impact underscored by its prevalence and devastating consequences. Whereas numerous oncogenes could contribute to cancer development, a group of transcription factors (TFs) are overactive in the majority of tumors. Targeting these TFs [...] Read more.
Cancer represents a significant and persistent global health burden, with its impact underscored by its prevalence and devastating consequences. Whereas numerous oncogenes could contribute to cancer development, a group of transcription factors (TFs) are overactive in the majority of tumors. Targeting these TFs may also combat the downstream oncogenes activated by the TFs, making them attractive potential targets for effective antitumor therapeutic strategy. One such TF is yin yang 1 (YY1), which plays crucial roles in the development and progression of various tumors. In preclinical studies, YY1 inhibition has shown efficacy in inhibiting tumor growth, promoting apoptosis, and sensitizing tumor cells to chemotherapy. Recent studies have also revealed the potential of combining YY1 inhibition with immunotherapy for enhanced antitumor effects. However, clinical translation of YY1-targeted therapy still faces challenges in drug specificity and delivery. This review provides an overview of YY1 biology, its role in tumor development and progression, as well as the strategies explored for YY1-targeted therapy, with a focus on their clinical implications, including those using small molecule inhibitors, RNA interference, and gene editing techniques. Finally, we discuss the challenges and current limitations of targeting YY1 and the need for further research in this area. Full article
(This article belongs to the Special Issue Pleiotropic Pro-tumor Activities Regulated by Overexpressed Yin Yang 1 (YY1) in Human Cancers: Clinical Implications)
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