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Cancers
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Genetic and Epigenetic Regulation of Tissue Homeostasis in Cancer
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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 11050

Special Issue Editors

Prof. Dr. Apostolos Klinakis

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Guest Editor
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
Dr. Theodoros Rampias

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Guest Editor
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
Dr. Panagiotis Karakaidos

E-Mail Website
Guest Editor
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 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

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Published Papers (4 papers)

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Research

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22 pages, 12727 KiB  
Article
Small Cajal Body-Specific RNA12 Promotes Carcinogenesis through Modulating Extracellular Matrix Signaling in Bladder Cancer
by Qinchen Lu, Jiandong Wang, Yuting Tao, Jialing Zhong, Zhao Zhang, Chao Feng, Xi Wang, Tianyu Li, Rongquan He, Qiuyan Wang and Yuanliang Xie
Cancers 2024, 16(3), 483; https://doi.org/10.3390/cancers16030483 - 23 Jan 2024
Cited by 1 | Viewed by 1667
Abstract
Background: Small Cajal body-specific RNAs (scaRNAs) are a specific subset of small nucleolar RNAs (snoRNAs) that have recently emerged as pivotal contributors in diverse physiological and pathological processes. However, their defined roles in carcinogenesis remain largely elusive. This study aims to explore the [...] Read more.
Background: Small Cajal body-specific RNAs (scaRNAs) are a specific subset of small nucleolar RNAs (snoRNAs) that have recently emerged as pivotal contributors in diverse physiological and pathological processes. However, their defined roles in carcinogenesis remain largely elusive. This study aims to explore the potential function and mechanism of SCARNA12 in bladder cancer (BLCA) and to provide a theoretical basis for further investigations into the biological functionalities of scaRNAs. Materials and Methods: TCGA, GEO and GTEx data sets were used to analyze the expression of SCARNA12 and its clinicopathological significance in BLCA. Quantitative real-time PCR (qPCR) and in situ hybridization were applied to validate the expression of SCARNA12 in both BLCA cell lines and tissues. RNA sequencing (RNA-seq) combined with bioinformatics analyses were conducted to reveal the changes in gene expression patterns and functional pathways in BLCA patients with different expressions of SCARNA12 and T24 cell lines upon SCARNA12 knockdown. Single-cell mass cytometry (CyTOF) was then used to evaluate the tumor-related cell cluster affected by SCARNA12. Moreover, SCARNA12 was stably knocked down in T24 and UMUC3 cell lines by lentivirus-mediated CRISPR/Cas9 approach. The biological effects of SCARNA12 on the proliferation, clonogenic, migration, invasion, cell apoptosis, cell cycle, and tumor growth were assessed by in vitro MTT, colony formation, wound healing, transwell, flow cytometry assays, and in vivo nude mice xenograft models, respectively. Finally, a chromatin isolation by RNA purification (ChIRP) experiment was further conducted to delineate the potential mechanisms of SCARNA12 in BLCA. Results: The expression of SCARNA12 was significantly up-regulated in both BLCA tissues and cell lines. RNA-seq data elucidated that SCARAN12 may play a potential role in cell adhesion and extracellular matrix (ECM) related signaling pathways. CyTOF results further showed that an ECM-related cell cluster with vimentin+, CD13+, CD44+, and CD47+ was enriched in BLCA patients with high SCARNA12 expression. Additionally, SCARNA12 knockdown significantly inhibited the proliferation, colony formation, migration, and invasion abilities in T24 and UMUC3 cell lines. SCARNA12 knockdown prompted cell arrest in the G0/G1 and G2/M phase and promoted apoptosis in T24 and UMUC3 cell lines. Furthermore, SCARNA12 knockdown could suppress the in vivo tumor growth in nude mice. A ChIRP experiment further suggested that SCARNA12 may combine transcription factors H2AFZ to modulate the transcription program and then affect BLCA progression. Conclusions: Our study is the first to propose aberrant alteration of SCARNA12 and elucidate its potential oncogenic roles in BLCA via the modulation of ECM signaling. The interaction of SCARNA12 with the transcriptional factor H2AFZ emerges as a key contributor to the carcinogenesis and progression of BLCA. These findings suggest SCARNA12 may serve as a diagnostic biomarker and potential therapeutic target for the treatment of BLCA. Full article
(This article belongs to the Special Issue Genetic and Epigenetic Regulation of Tissue Homeostasis in Cancer)
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14 pages, 3843 KiB  
Article
Cancer-Associated Stromal Cells Promote the Contribution of MMP2-Positive Bone Marrow-Derived Cells to Oral Squamous Cell Carcinoma Invasion
by May Wathone Oo, Hotaka Kawai, Kiyofumi Takabatake, Qiusheng Shan, Htoo Shwe Eain, Shintaro Sukegawa, Keisuke Nakano and Hitoshi Nagatsuka
Cancers 2022, 14(1), 137; https://doi.org/10.3390/cancers14010137 - 28 Dec 2021
Cited by 4 | Viewed by 2362
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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19 pages, 1518 KiB  
Review
OGG1 as an Epigenetic Reader Affects NFκB: What This Means for Cancer
by Spiros Vlahopoulos, Lang Pan, Lokman Varisli, Garrett M. Dancik, Theodoros Karantanos and Istvan Boldogh
Cancers 2024, 16(1), 148; https://doi.org/10.3390/cancers16010148 - 28 Dec 2023
Cited by 1 | Viewed by 2403
Abstract
8-oxoguanine glycosylase 1 (OGG1), which was initially identified as the enzyme that catalyzes the first step in the DNA base excision repair pathway, is now also recognized as a modulator of gene expression. What is important for cancer is that OGG1 acts as [...] Read more.
8-oxoguanine glycosylase 1 (OGG1), which was initially identified as the enzyme that catalyzes the first step in the DNA base excision repair pathway, is now also recognized as a modulator of gene expression. What is important for cancer is that OGG1 acts as a modulator of NFκB-driven gene expression. Specifically, oxidant stress in the cell transiently halts enzymatic activity of substrate-bound OGG1. The stalled OGG1 facilitates DNA binding of transactivators, such as NFκB to their cognate sites, enabling the expression of cytokines and chemokines, with ensuing recruitment of inflammatory cells. Recently, we highlighted chief aspects of OGG1 involvement in regulation of gene expression, which hold significance in lung cancer development. However, OGG1 has also been implicated in the molecular underpinning of acute myeloid leukemia. This review analyzes and discusses how these cells adapt through redox-modulated intricate connections, via interaction of OGG1 with NFκB, which provides malignant cells with alternative molecular pathways to transform their microenvironment, enabling adjustment, promoting cell proliferation, metastasis, and evading killing by therapeutic agents. Full article
(This article belongs to the Special Issue Genetic and Epigenetic Regulation of Tissue Homeostasis in Cancer)
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24 pages, 2161 KiB  
Review
Typical Enhancers, Super-Enhancers, and Cancers
by Marianna A. Koutsi, Marialena Pouliou, Lydia Champezou, Giannis Vatsellas, Angeliki-Ioanna Giannopoulou, Christina Piperi and Marios Agelopoulos
Cancers 2022, 14(18), 4375; https://doi.org/10.3390/cancers14184375 - 8 Sep 2022
Cited by 12 | Viewed by 3800
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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