Special Issue "Genetic and Epigenetic Regulation of Tissue Homeostasis in Cancer"

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

Deadline for manuscript submissions: closed (31 May 2023) | Viewed by 4575

Special Issue Editors

Cancer Biology Group, Biomedical Research Foundation of the Academy of Athens, 4 Soranou Efesiou, 11527 Athens, Greece
Interests: cancer; cell signaling; epigenetics; tissue homeostasis; therapeutic response
Biomedical Research Foundation of the Academy of Athens (BRFAA), 11741 Athens, Greece
Interests: genome integrity; epigenetic regulation; gene expression; translation; viruses; molecular virology; viruses’ evolution
Special Issues, Collections and Topics in MDPI journals
Cancer Biology Group, Biomedical Research Foundation of the Academy of Athens, 4 Soranou Efesiou, 11527 Athens, Greece
Interests: cancer; cancer stem cells; epigenetics

Special Issue Information

Dear Colleagues,

Epithelial tissues represent the dynamic barriers between the external environment and internal surfaces of our bodies. This vital function requires extended networks of cell–cell and cell–extracellular matrix interactions which stabilize tissues but also facilitate communication with the microenvironment. To support tissue homeostasis and injury-induced repair, a hierarchical cellular architecture, with tissue-specific stem/progenitor cells, differentiating into a whole range of specialized cells is maintained and tightly regulated. These tissue homeostasis processes are driven and defined by specific transcriptional and epigenetic landscapes that determine the cellular identity within tissue. As a result, epithelial integrity and homeostasis are safeguarded by a finely tuned balance between proliferation and differentiation. Similar principles apply to nonepithelial tissues, including the nervous system, the hemopoietic system and endothelial and stromal tissues.

Early stages of carcinogenesis are characterized by genomic and epigenetic alterations that lead to tissue disorganization, as poorly differentiated transformed cells exhibit a marked loss of traits associated with epithelial integrity.

For this Special Issue of Cancers, we invite authors to submit contributions that provide novel findings in the field of cancer progression in epithelia. In particular (though not limited to), insights in developmental pathways, epigenetic and transcriptional changes, tissue repair and regeneration, extracellular matrix–epithelial cell communication, with respect to loss of epithelial integrity during early phases of carcinogenesis, are of great interest. Reviews that highlight new findings in the above areas are also welcome.

Dr. Apostolos Klinakis
Dr. Theodoros Rampias
Dr. Panagiotis Karakaidos
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 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

  • stem cells
  • tissue integrity
  • tissue homeostasis
  • tissue repair
  • tissue microenvironment
  • signaling imbalance
  • developmental pathways in cancer
  • epigenetics
  • cancer stem cells
  • tumor microenvironment

Published Papers (2 papers)

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Research

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Article
Cancer-Associated Stromal Cells Promote the Contribution of MMP2-Positive Bone Marrow-Derived Cells to Oral Squamous Cell Carcinoma Invasion
Cancers 2022, 14(1), 137; https://doi.org/10.3390/cancers14010137 - 28 Dec 2021
Cited by 3 | Viewed by 1650
Abstract
Tumor stromal components contribute to tumor development and invasion. However, the role of stromal cells in the contribution of bone marrow-derived cells (BMDCs) in oral squamous cell carcinoma (OSCC) invasion is unclear. In the present study, we created two different invasive OSCC patient-derived [...] Read more.
Tumor stromal components contribute to tumor development and invasion. However, the role of stromal cells in the contribution of bone marrow-derived cells (BMDCs) in oral squamous cell carcinoma (OSCC) invasion is unclear. In the present study, we created two different invasive OSCC patient-derived stroma xenografts (PDSXs) and analyzed and compared the effects of stromal cells on the relation of BMDCs and tumor invasion. We isolated stromal cells from two OSCC patients: less invasive verrucous OSCC (VSCC) and highly invasive conventional OSCC (SCC) and co-xenografted with the OSCC cell line (HSC-2) on green fluorescent protein (GFP)-positive bone marrow (BM) cells transplanted mice. We traced the GFP-positive BM cells by immunohistochemistry (IHC) and detected matrix metalloproteinase 2 (MMP2) expression on BM cells by double fluorescent IHC. The results indicated that the SCC-PDSX promotes MMP2-positive BMDCs recruitment to the invasive front line of the tumor. Furthermore, microarray analysis revealed that the expressions of interleukin 6; IL-6 mRNA and interleukin 1 beta; IL1B mRNA were higher in SCC stromal cells than in VSCC stromal cells. Thus, our study first reports that IL-6 and IL1B might be the potential stromal factors promoting the contribution of MMP2-positive BMDCs to OSCC invasion. Full article
(This article belongs to the Special Issue Genetic and Epigenetic Regulation of Tissue Homeostasis in Cancer)
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Review

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Review
Typical Enhancers, Super-Enhancers, and Cancers
Cancers 2022, 14(18), 4375; https://doi.org/10.3390/cancers14184375 - 08 Sep 2022
Cited by 1 | Viewed by 2434
Abstract
Non-coding segments of the human genome are enriched in cis-regulatory modules that constitute functional elements, such as transcriptional enhancers and Super-enhancers. A hallmark of cancer pathogenesis is the dramatic dysregulation of the “archetype” gene expression profiles of normal human cells. Genomic variations [...] Read more.
Non-coding segments of the human genome are enriched in cis-regulatory modules that constitute functional elements, such as transcriptional enhancers and Super-enhancers. A hallmark of cancer pathogenesis is the dramatic dysregulation of the “archetype” gene expression profiles of normal human cells. Genomic variations can promote such deficiencies when occurring across enhancers and Super-enhancers, since they affect their mechanistic principles, their functional capacity and specificity, and the epigenomic features of the chromatin microenvironment across which these regulatory elements reside. Here, we comprehensively describe: fundamental mechanisms of gene expression dysregulation in cancers that involve genomic abnormalities within enhancers’ and Super-enhancers’ (SEs) sequences, which alter the expression of oncogenic transcription factors (TFs); cutting-edge technologies applied for the analysis of variation-enriched hotspots of the cancer genome; and pharmacological approaches for the treatment of Super-enhancers’ aberrant function. Finally, we provide an intratumor meta-analysis, which highlights that genomic variations in transcription-factor-driven tumors are accompanied overexpression of genes, a portion of which encodes for additional cancer-related transcription factors. Full article
(This article belongs to the Special Issue Genetic and Epigenetic Regulation of Tissue Homeostasis in Cancer)
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