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Cancers
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Cell Plasticity in Cancer Progression
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Cell Plasticity in Cancer Progression

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

Deadline for manuscript submissions: closed (30 April 2023) | Viewed by 21027

Special Issue Editors

Dr. Orlando Musso

E-Mail Website
Guest Editor
Inserm, UMR991, Liver Metabolisms and Cancer, Rennes, France
Université de Rennes 1, F-35043 Rennes, France
Interests: Exogenous and Endogenous Stress and Pathological Responses in Hepato-Gastrointestinal Diseases
Dr. Anne Corlu

E-Mail Website
Co-Guest Editor
Research Director, Tenure position, Centre National de la Recherche Scientifique (CNRS) - Institut NuMeCan (Nutrition, Metabolism and Cancer), INSERM U1241, Univ Rennes, INRAe, F-35000 Rennes, France
Interests: cancer; hepatocyte differentiation; cancer stem cells; cell plasticity; liver regeneration; hepatocellular; carcinoma; inflammation; cancer cell metabolism
Dr. Bruno Clément

E-Mail Website
Co-Guest Editor
Research Director, Tenure Position, French National Institute of Health and Medical Research (INSERM) - Institut NuMeCan (Nutrition, Metabolism and Cancer), INSERM U1241, Univ Rennes, INRAe, Rennes, Brittany, France
Interests: extracellular matrix; cancer; French National Liver Cancer Network; bioresources; liver metabolism

Special Issue Information

Dear Colleagues,

Cancer cell plasticity generates heterogeneity and fosters the survival of the fittest tumor cells. From preneoplastic lesions through invasive cancers, cells acquire evolutive nuclear and cytoplasmic features that result from groundbreaking genetic and epigenetic reprogramming. Cancer overturns the balance between cell proliferation and differentiation, which leads to a breakdown of tissue scaffolds with the loss of normal tissue architecture. This process is well illustrated by the progression from mild epithelial dysplasia to infiltrating carcinomas, whereby the expansion of the basal cell layer takes over the whole thickness of the epithelium before the cancer cells break through extracellular matrix barriers, reach capillary vessels and disseminate systemically. Three major and related features of cancer cell biology underlie these changes: reversible epithelial-to-mesenchymal transition, the amplification of the cancer stem cell contingent, and adaptive energy metabolism. These features concur to generate new cancer cells with proliferative, migratory, invasive and/or adhesive capacities and a spectrum of progenitor cell lineages that provide genetic and phenotypic diversity. Although the cost of plasticity is the de novo expression of oncofetal immunogens, cancer cells circumvent their immunogenicity by evading the host’s innate and adaptive immunity. This Special Issue presents cell plasticity as a set of coevolving functional networks underlying a dynamic, adaptive equilibrium.

Dr. Orlando Musso
Dr. Anne Corlu
Dr. Bruno Clément
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

  • cancer cell plasticity
  • heterogeneity
  • cancer stem cell

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Published Papers (5 papers)

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Research

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15 pages, 4107 KiB  
Article
Expression of Extracellular Matrix-Related Genes and Their Regulatory microRNAs in Problematic Colorectal Polyps
by Margareta Žlajpah, Emanuela Boštjančič, Bojan Tepeš and Nina Zidar
Cancers 2020, 12(12), 3715; https://doi.org/10.3390/cancers12123715 - 11 Dec 2020
Cited by 2 | Viewed by 2363
Abstract
Colorectal carcinoma usually evolves gradually, forming a spectrum of lesions, due to accumulation of genetic mutations and epigenetic alterations. Many early lesions are detected since the introduction of screening programs. The greatest challenge is to distinguish between adenomas with epithelial misplacement (AEM) and [...] Read more.
Colorectal carcinoma usually evolves gradually, forming a spectrum of lesions, due to accumulation of genetic mutations and epigenetic alterations. Many early lesions are detected since the introduction of screening programs. The greatest challenge is to distinguish between adenomas with epithelial misplacement (AEM) and adenomas with early carcinoma (AEC), considering the diagnosis affects prognosis and treatment. We analyzed the expression of selected extracellular matrix (ECM)-related genes and proteins, and their regulatory microRNAs using RT-qPCR and immunohistochemistry in biopsies from 44 patients. Differences were observed in AEM in comparison to AEC for DCN, EPHA4, FN1, SPON2, and SPP1, reflecting inflammatory stromal reaction to traumatisation and misplacement of dysplastic glands in the submucosa in the former, and desmoplastic stromal reaction to true invasion of dysplastic glands in the submucosa in the latter. Expression of regulatory microRNAs hsa-miR-200c and hsa-miR-146a significantly negatively correlated with the expression of their regulated genes, while significant difference between AEM and AEC was observed only for hsa-miR-29c. The described expression patterns are too complex to be used in diagnostic work, but might contribute to better understanding ECM changes in colorectal carcinoma development, helping to find new markers in the future. Full article
(This article belongs to the Special Issue Cell Plasticity in Cancer Progression)
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Review

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23 pages, 4375 KiB  
Review
Cellular Plasticity in Mammary Gland Development and Breast Cancer
by Madison N. Wicker and Kay-Uwe Wagner
Cancers 2023, 15(23), 5605; https://doi.org/10.3390/cancers15235605 - 27 Nov 2023
Cited by 4 | Viewed by 2788
Abstract
Cellular plasticity is a phenomenon where cells adopt different identities during development and tissue homeostasis as a response to physiological and pathological conditions. This review provides a general introduction to processes by which cells change their identity as well as the current definition [...] Read more.
Cellular plasticity is a phenomenon where cells adopt different identities during development and tissue homeostasis as a response to physiological and pathological conditions. This review provides a general introduction to processes by which cells change their identity as well as the current definition of cellular plasticity in the field of mammary gland biology. Following a synopsis of the evolving model of the hierarchical development of mammary epithelial cell lineages, we discuss changes in cell identity during normal mammary gland development with particular emphasis on the effect of the gestation cycle on the emergence of new cellular states. Next, we summarize known mechanisms that promote the plasticity of epithelial lineages in the normal mammary gland and highlight the importance of the microenvironment and extracellular matrix. A discourse of cellular reprogramming during the early stages of mammary tumorigenesis that follows focuses on the origin of basal-like breast cancers from luminal progenitors and oncogenic signaling networks that orchestrate diverse developmental trajectories of transforming epithelial cells. In addition to the epithelial-to-mesenchymal transition, we highlight events of cellular reprogramming during breast cancer progression in the context of intrinsic molecular subtype switching and the genesis of the claudin-low breast cancer subtype, which represents the far end of the spectrum of epithelial cell plasticity. In the final section, we will discuss recent advances in the design of genetically engineered models to gain insight into the dynamic processes that promote cellular plasticity during mammary gland development and tumorigenesis in vivo. Full article
(This article belongs to the Special Issue Cell Plasticity in Cancer Progression)
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35 pages, 1440 KiB  
Review
Molecular Crosstalk between the Hepatitis C Virus and the Extracellular Matrix in Liver Fibrogenesis and Early Carcinogenesis
by Emma Reungoat, Boyan Grigorov, Fabien Zoulim and Eve-Isabelle Pécheur
Cancers 2021, 13(9), 2270; https://doi.org/10.3390/cancers13092270 - 9 May 2021
Cited by 12 | Viewed by 3503
Abstract
Chronic infection by the hepatitis C virus (HCV) is a major cause of liver diseases, predisposing to fibrosis and hepatocellular carcinoma. Liver fibrosis is characterized by an overly abundant accumulation of components of the hepatic extracellular matrix, such as collagen and elastin, with [...] Read more.
Chronic infection by the hepatitis C virus (HCV) is a major cause of liver diseases, predisposing to fibrosis and hepatocellular carcinoma. Liver fibrosis is characterized by an overly abundant accumulation of components of the hepatic extracellular matrix, such as collagen and elastin, with consequences on the properties of this microenvironment and cancer initiation and growth. This review will provide an update on mechanistic concepts of HCV-related liver fibrosis/cirrhosis and early stages of carcinogenesis, with a dissection of the molecular details of the crosstalk during disease progression between hepatocytes, the extracellular matrix, and hepatic stellate cells. Full article
(This article belongs to the Special Issue Cell Plasticity in Cancer Progression)
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17 pages, 1308 KiB  
Review
Interplay between Metabolism Reprogramming and Epithelial-to-Mesenchymal Transition in Cancer Stem Cells
by Yoann Daniel, Elise Lelou, Caroline Aninat, Anne Corlu and Florian Cabillic
Cancers 2021, 13(8), 1973; https://doi.org/10.3390/cancers13081973 - 20 Apr 2021
Cited by 24 | Viewed by 6113
Abstract
Tumor cells display important plasticity potential, which contributes to intratumoral heterogeneity. Notably, tumor cells have the ability to retrodifferentiate toward immature states under the influence of their microenvironment. Importantly, this phenotypical conversion is paralleled by a metabolic rewiring, and according to the metabostemness [...] Read more.
Tumor cells display important plasticity potential, which contributes to intratumoral heterogeneity. Notably, tumor cells have the ability to retrodifferentiate toward immature states under the influence of their microenvironment. Importantly, this phenotypical conversion is paralleled by a metabolic rewiring, and according to the metabostemness theory, metabolic reprogramming represents the first step of epithelial-to-mesenchymal transition (EMT) and acquisition of stemness features. Most cancer stem cells (CSC) adopt a glycolytic phenotype even though cells retain functional mitochondria. Such adaptation is suggested to reduce the production of reactive oxygen species (ROS), protecting CSC from detrimental effects of ROS. CSC may also rely on glutaminolysis or fatty acid metabolism to sustain their energy needs. Besides pro-inflammatory cytokines that are well-known to initiate the retrodifferentiation process, the release of catecholamines in the microenvironment of the tumor can modulate both EMT and metabolic changes in cancer cells through the activation of EMT transcription factors (ZEB1, Snail, or Slug (SNAI2)). Importantly, the acquisition of stem cell properties favors the resistance to standard care chemotherapies. Hence, a better understanding of this process could pave the way for the development of therapies targeting CSC metabolism, providing new strategies to eradicate the whole tumor mass in cancers with unmet needs. Full article
(This article belongs to the Special Issue Cell Plasticity in Cancer Progression)
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18 pages, 3049 KiB  
Review
ADAM and ADAMTS Proteins, New Players in the Regulation of Hepatocellular Carcinoma Microenvironment
by Nathalie Théret, Fidaa Bouezzeddine, Fida Azar, Mona Diab-Assaf and Vincent Legagneux
Cancers 2021, 13(7), 1563; https://doi.org/10.3390/cancers13071563 - 29 Mar 2021
Cited by 23 | Viewed by 5199
Abstract
The tumor microenvironment plays a major role in tumor growth, invasion and resistance to chemotherapy, however understanding how all actors from microenvironment interact together remains a complex issue. The tumor microenvironment is classically represented as three closely connected components including the stromal cells [...] Read more.
The tumor microenvironment plays a major role in tumor growth, invasion and resistance to chemotherapy, however understanding how all actors from microenvironment interact together remains a complex issue. The tumor microenvironment is classically represented as three closely connected components including the stromal cells such as immune cells, fibroblasts, adipocytes and endothelial cells, the extracellular matrix (ECM) and the cytokine/growth factors. Within this space, proteins of the adamalysin family (ADAM for a disintegrin and metalloproteinase; ADAMTS for ADAM with thrombospondin motifs; ADAMTSL for ADAMTS-like) play critical roles by modulating cell–cell and cell–ECM communication. During last decade, the implication of adamalysins in the development of hepatocellular carcinoma (HCC) has been supported by numerous studies however the functional characterization of most of them remain unsettled. In the present review we propose both an overview of the literature and a meta-analysis of adamalysins expression in HCC using data generated by The Cancer Genome Atlas (TCGA) Research Network. Full article
(This article belongs to the Special Issue Cell Plasticity in Cancer Progression)
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