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CelebratING 25 Years of the ING Family Proteins as Epigenetic...
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CelebratING 25 Years of the ING Family Proteins as Epigenetic Regulators in Cancer

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: closed (31 July 2023) | Viewed by 10972

Special Issue Editors

Prof. Dr. Karl Riabowol

E-Mail Website
Guest Editor
Arnie Charbonneau Cancer Institute and Alberta Children’s Hospital Research Institute, University of Calgary, 3330 Hospital Drive NW, Calgary, Alberta T2N 4N1, Canada
Interests: Function of Tumour Suppressors and Epigenetic Regulators in Cancer and Ageing
Prof. Dr. Gesche Tallen

E-Mail Website
Guest Editor
Alberta Children’s Hospital Research Institute, Department of Oncology, Cumming School of Medicine, University of Calgary, Calgary, Alberta T2N 4N1, Canada
Department of Paediatrics, Hematology-Oncology-Transplant (HOT)-Program, Alberta Children’s Hospital, 28 Oki Drive N.W., Calgary, Alberta T3B 6A8, Canada
Interests: Pediatric (Neuro-)Oncology; Long-Term Sequelae in Childhood Cancer Survivors

Special Issue Information

Dear Colleagues,

We would like to introduce a Special Issue of the journal Cancers, titled "CelebratING 25 years of the ING family proteins as epigenetic regulators in cancer".

Cancer cells accumulate genetic and epigenetic changes that alter gene expression to drive tumorigenesis. The epigenetic silencing of tumor suppressor, cell cycle, differentiation and DNA repair genes contributes to neoplastic transformation.

The founding member of the ING (inhibitor of growth) family, ING1, was discovered in 1996 by PCR-mediated subtractive hybridization using cDNAs from a normal mammary epithelial cell strain and several transformed breast cancer cell lines, followed by an in vivo functional screen to identify differentially expressed factors impacting tumorigenesis. Back then, the overexpression of ectopic ING1 was observed to promote cell cycle arrest or apoptosis, while the inhibition of its expression with antisense RNA led to cellular transformation in vitro and tumor formation in vivo. Subsequently, four more ING proteins (ING2–ING5) were identified in mammals based on sequence homology to ING1.

Over the past 25 years, ING1–ING5 have been described as a multifaceted family of growth and senescence regulators, DNA repair modulators, phospholipid effectors, histone mark sensors and core components of HDAC1/2, several HAT chromatin-modifying complexes and governors of stem cell differentiation.

This Special Issue will provide the most current insights into ING structure, the pathways by which ING family proteins differentially affect the Hallmarks of Cancer and highlight the various epigenetic mechanisms by which they regulate gene expression and may serve as biomarkers and therapeutic targets in future epigenetic treatment strategies for cancer patients.

Prof. Dr. Karl Riabowol
Prof. Dr. Gesche Tallen
Guest Editors

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 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

  • ING Proteins
  • Epigenetic Readers
  • Histone Acetylation
  • Tumour Suppressors
  • Stem Cells
  • PHD
  • Chromatin
  • DNA Repair

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Published Papers (3 papers)

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Research

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17 pages, 3123 KiB  
Article
Loss of ING3 in the Prostate Leads to Activation of DNA Damage Repair Markers
by Viktor Lang, Lisa Barones, ShiTing Misaki Hu, Fatemeh Hashemi, Karen Blote, Karl Riabowol and Dieter Fink
Cancers 2025, 17(6), 1037; https://doi.org/10.3390/cancers17061037 - 20 Mar 2025
Viewed by 1868
Abstract
Background/Objectives: The inhibitor of growth family member 3 (ING3) acts as an epigenetic reader through physical interactions with histone-modifying enzymes and subsequent chromatin remodelling processes. It is involved in various cellular functions, such as cell cycle control, cell growth, and apoptosis. Although ING3 [...] Read more.
Background/Objectives: The inhibitor of growth family member 3 (ING3) acts as an epigenetic reader through physical interactions with histone-modifying enzymes and subsequent chromatin remodelling processes. It is involved in various cellular functions, such as cell cycle control, cell growth, and apoptosis. Although ING3 was assigned tumour suppressor candidate status in some types of cancers, including prostate cancer, some studies suggest it acts to promote growth. To address these contradictory reports regarding its role in the initiation and progression of prostate cancer, we specifically addressed the question of whether ablation of ING3 in the mouse prostate is sufficient to initiate malignant transformation of the prostate and support its (candidate) tumour suppressor status. Methods: To generate the prostate-specific Ing3 knockout mouse, paternal inheritance of the PB-Cre4 transgene was used, while for the generation of a global knockout control, a female mouse harbouring the PB-Cre4 transgene was utilized. To determine the recombination efficiency of the Cre-LoxP system in the prostate at the Ing3 locus, a duplex probe-based digital PCR assay capable of counting undisrupted Ing3 copies was designed. The impact of DNA recombination on the protein level was investigated by immunohistochemical staining of prostate tissue samples. Results: In the prostate-specific knockout, digital PCR analysis revealed mosaic gene deletion. We found recombination efficiencies in the anterior, dorsolateral, and ventral prostate lobes ranging from approximately 15 to 30%. ING3 staining in the prostate was faint with no detectable differences in signal intensity between the knockout specimen and wild-type controls. This low ING3 expression in the prostate is consistent with observations of X-gal staining of an Ing3-LacZ reporter allele. Immunohistochemistry showed increased expression of DNA-damage-associated markers γH2AX and 53BP1. However, no gross anatomical abnormalities or prostate intraepithelial neoplasia (PIN) lesions in the prostate of tissue-specific knockout animals compared to wild-type controls were observed. Conclusions: Altogether, our data provide evidence that disruption of ING3 expression in prostate cells does not lead to malignant transformation and challenges the idea that ING3 acts primarily in a tumour-suppressive manner. Furthermore, this work supports the crucial role of ING3 in maintaining genomic stability, and we confirmed the embryonic lethal phenotype of homozygous Ing3 null mice that is rescued by ectopic expression of ING3. Full article
(This article belongs to the Special Issue CelebratING 25 Years of the ING Family Proteins as Epigenetic Regulators in Cancer)
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Review

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18 pages, 1944 KiB  
Review
BRPF1-KAT6A/KAT6B Complex: Molecular Structure, Biological Function and Human Disease
by Gaoyu Zu, Ying Liu, Jingli Cao, Baicheng Zhao, Hang Zhang and Linya You
Cancers 2022, 14(17), 4068; https://doi.org/10.3390/cancers14174068 - 23 Aug 2022
Cited by 14 | Viewed by 6202
Abstract
The bromodomain and PHD finger–containing protein1 (BRPF1) is a member of family IV of the bromodomain-containing proteins that participate in the post-translational modification of histones. It functions in the form of a tetrameric complex with a monocytic leukemia zinc finger protein (MOZ or [...] Read more.
The bromodomain and PHD finger–containing protein1 (BRPF1) is a member of family IV of the bromodomain-containing proteins that participate in the post-translational modification of histones. It functions in the form of a tetrameric complex with a monocytic leukemia zinc finger protein (MOZ or KAT6A), MOZ-related factor (MORF or KAT6B) or HAT bound to ORC1 (HBO1 or KAT7) and two small non-catalytic proteins, the inhibitor of growth 5 (ING5) or the paralog ING4 and MYST/Esa1-associated factor 6 (MEAF6). Mounting studies have demonstrated that all the four core subunits play crucial roles in different biological processes across diverse species, such as embryonic development, forebrain development, skeletal patterning and hematopoiesis. BRPF1, KAT6A and KAT6B mutations were identified as the cause of neurodevelopmental disorders, leukemia, medulloblastoma and other types of cancer, with germline mutations associated with neurodevelopmental disorders displaying intellectual disability, and somatic variants associated with leukemia, medulloblastoma and other cancers. In this paper, we depict the molecular structures and biological functions of the BRPF1-KAT6A/KAT6B complex, summarize the variants of the complex related to neurodevelopmental disorders and cancers and discuss future research directions and therapeutic potentials. Full article
(This article belongs to the Special Issue CelebratING 25 Years of the ING Family Proteins as Epigenetic Regulators in Cancer)
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12 pages, 1464 KiB  
Review
Inhibitor of Growth Factors Regulate Cellular Senescence
by Soudeh Ghafouri-Fard, Mohammad Taheri and Aria Baniahmad
Cancers 2022, 14(13), 3107; https://doi.org/10.3390/cancers14133107 - 24 Jun 2022
Cited by 3 | Viewed by 2179
Abstract
The Inhibitor of Growth (ING) proteins are a group of tumor suppressors with five conserved genes. A common motif of ING factors is the conserved plant homeodomain (PHD), with which they bind to chromatin as readers of the histone mark trimethylated histone H3 [...] Read more.
The Inhibitor of Growth (ING) proteins are a group of tumor suppressors with five conserved genes. A common motif of ING factors is the conserved plant homeodomain (PHD), with which they bind to chromatin as readers of the histone mark trimethylated histone H3 (H3K4me3). These genes often produce several protein products through alternative splicing events. Interestingly, ING1 and ING2 participate in the establishment of the repressive mSIN3a-HDAC complexes, whereas ING3, ING4, and ING5 are associated with the activating HAT protein complexes. In addition to the modulation of chromatin’s structure, they regulate cell cycle transition, cellular senescence, repair of DNA damage, apoptosis, and angiogenic pathways. They also have fundamental effects on regulating cellular senescence in cancer cells. In the current review, we explain their role in cellular senescence based on the evidence obtained from cell line and animal studies, particularly in the context of cancer. Full article
(This article belongs to the Special Issue CelebratING 25 Years of the ING Family Proteins as Epigenetic Regulators in Cancer)
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