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Cancers
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Molecular Mechanism of the Interaction Between Cells and Extracellular Matrix...
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Molecular Mechanism of the Interaction Between Cells and Extracellular Matrix in Cancer Progression

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

Deadline for manuscript submissions: closed (30 September 2022) | Viewed by 18630

Special Issue Editors

Dr. Suzanne Ponik

E-Mail Website
Guest Editor
Department of Cell and Regenerative Biology, Wisconsin Institutes for Medical Research, University of Wisconsin-Madison, Madison, WI, USA
Interests: breast cancer; extracellular matrix; cell adhesion and migration; metastasis
Dr. Seiichiro Ishihara

E-Mail Website
Guest Editor
Department of Advanced Transdisciplinary Sciences, Faculty of Advanced Life Science, Hokkaido University, Sapporo, Japan
Interests: Cancer Biology; Cell Biology; Mechanobiology

Special Issue Information

Dear Colleagues,

During solid tumor progression, aberrant changes in extracellular matrix (ECM) composition and organization diversify the three-dimensional spatial topography of biochemical and biophysical properties that impact cellular behavior. To survive and disseminate, cancer cells rely on their ability to sense changes in the microenvironment and respond by dynamically remodeling the surrounding ECM.

This Special Issue of Cancers will focus on how the dynamic reciprocity between cells and their microenvironment, that is, the interactions between tumor, stromal cells, and the ECM, impacts tumor progression. We welcome research papers as well as expert reviews that are focused on, but are not limited to, the study of the molecular mechanisms underlying the dynamic reciprocity involved in: a) generating hospitable microenvironments within the primary tumor or metastatic niche; b) priming tumor cells for dormancy or metastatic growth; c) developing drug resistance.

Dr. Suzanne Ponik
Dr. Seiichiro Ishihara
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

  • cancer progression
  • extracellular matrix
  • mechano-signaling
  • matrix remodeling
  • metastatic niche
  • dormancy
  • metastasis
  • drug resistance

Published Papers (5 papers)

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Research

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22 pages, 4863 KiB  
Article
PRELP Regulates Cell–Cell Adhesion and EMT and Inhibits Retinoblastoma Progression
by Jack Hopkins, Ken Asada, Alex Leung, Vasiliki Papadaki, Hongorzul Davaapil, Matthew Morrison, Tomoko Orita, Ryohei Sekido, Hirofumi Kosuge, M. Ashwin Reddy, Kazuhiro Kimura, Akihisa Mitani, Kouhei Tsumoto, Ryuji Hamamoto, Mandeep S. Sagoo and Shin-ichi Ohnuma
Cancers 2022, 14(19), 4926; https://doi.org/10.3390/cancers14194926 - 08 Oct 2022
Cited by 5 | Viewed by 1999
Abstract
Retinoblastoma (RB) is the most common intraocular pediatric cancer. Nearly all cases of RB are associated with mutations compromising the function of the RB1 tumor suppressor gene. We previously demonstrated that PRELP is widely downregulated in various cancers and our in vivo and [...] Read more.
Retinoblastoma (RB) is the most common intraocular pediatric cancer. Nearly all cases of RB are associated with mutations compromising the function of the RB1 tumor suppressor gene. We previously demonstrated that PRELP is widely downregulated in various cancers and our in vivo and in vitro analysis revealed PRELP as a novel tumor suppressor and regulator of EMT. In addition, PRELP is located at chromosome 1q31.1, around a region hypothesized to be associated with the initiation of malignancy in RB. Therefore, in this study, we investigated the role of PRELP in RB through in vitro analysis and next-generation sequencing. Immunostaining revealed that PRELP is expressed in Müller glial cells in the retina. mRNA expression profiling of PRELP−/− mouse retina and PRELP-treated RB cells found that PRELP contributes to RB progression via regulation of the cancer microenvironment, in which loss of PRELP reduces cell–cell adhesion and facilitates EMT. Our observations suggest that PRELP may have potential as a new strategy for RB treatment. Full article
(This article belongs to the Special Issue Molecular Mechanism of the Interaction Between Cells and Extracellular Matrix in Cancer Progression)
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24 pages, 9385 KiB  
Article
Temozolomide-Acquired Resistance Is Associated with Modulation of the Integrin Repertoire in Glioblastoma, Impact of α5β1 Integrin
by Saidu Sani, Nikita Pallaoro, Mélissa Messe, Chloé Bernhard, Nelly Etienne-Selloum, Horst Kessler, Luciana Marinelli, Natacha Entz-Werle, Sophie Foppolo, Sophie Martin, Damien Reita and Monique Dontenwill
Cancers 2022, 14(2), 369; https://doi.org/10.3390/cancers14020369 - 12 Jan 2022
Cited by 3 | Viewed by 2247
Abstract
Despite extensive treatment, glioblastoma inevitably recurs, leading to an overall survival of around 16 months. Understanding why and how tumours resist to radio/chemotherapies is crucial to overcome this unmet oncological challenge. Primary and acquired resistance to Temozolomide (TMZ), the standard-of-care chemotherapeutic drug, have [...] Read more.
Despite extensive treatment, glioblastoma inevitably recurs, leading to an overall survival of around 16 months. Understanding why and how tumours resist to radio/chemotherapies is crucial to overcome this unmet oncological challenge. Primary and acquired resistance to Temozolomide (TMZ), the standard-of-care chemotherapeutic drug, have been the subjects of several studies. This work aimed to evaluate molecular and phenotypic changes occurring during and after TMZ treatment in a glioblastoma cell model, the U87MG. These initially TMZ-sensitive cells acquire long-lasting resistance even after removal of the drug. Transcriptomic analysis revealed that profound changes occurred between parental and resistant cells, particularly at the level of the integrin repertoire. Focusing on α5β1 integrin, which we proposed earlier as a glioblastoma therapeutic target, we demonstrated that its expression was decreased in the presence of TMZ but restored after removal of the drug. In this glioblastoma model of recurrence, α5β1 integrin plays an important role in the proliferation and migration of tumoral cells. We also demonstrated that reactivating p53 by MDM2 inhibitors concomitantly with the inhibition of this integrin in recurrent cells may overcome the TMZ resistance. Our results may explain some integrin-based targeted therapy failure as integrin expressions are highly switchable during the time of treatment. We also propose an alternative way to alter the viability of recurrent glioblastoma cells expressing a high level of α5β1 integrin. Full article
(This article belongs to the Special Issue Molecular Mechanism of the Interaction Between Cells and Extracellular Matrix in Cancer Progression)
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20 pages, 8483 KiB  
Article
Obesity-Activated Lung Stromal Cells Promote Myeloid Lineage Cell Accumulation and Breast Cancer Metastasis
by Lauren E. Hillers-Ziemer, Abbey E. Williams, Amanda Janquart, Caitlin Grogan, Victoria Thompson, Adriana Sanchez and Lisa M. Arendt
Cancers 2021, 13(5), 1005; https://doi.org/10.3390/cancers13051005 - 28 Feb 2021
Cited by 9 | Viewed by 2757
Abstract
Obesity is correlated with increased incidence of breast cancer metastasis; however, the mechanisms underlying how obesity promotes metastasis are unclear. In a diet-induced obese mouse model, obesity enhanced lung metastasis in both the presence and absence of primary mammary tumors and increased recruitment [...] Read more.
Obesity is correlated with increased incidence of breast cancer metastasis; however, the mechanisms underlying how obesity promotes metastasis are unclear. In a diet-induced obese mouse model, obesity enhanced lung metastasis in both the presence and absence of primary mammary tumors and increased recruitment of myeloid lineage cells into the lungs. In the absence of tumors, obese mice demonstrated increased numbers of myeloid lineage cells and elevated collagen fibers within the lung stroma, reminiscent of premetastatic niches formed by primary tumors. Lung stromal cells isolated from obese tumor-naïve mice showed increased proliferation, contractility, and expression of extracellular matrix, inflammatory markers and transforming growth factor beta-1 (TGFβ1). Conditioned media from lung stromal cells from obese mice promoted myeloid lineage cell migration in vitro in response to colony-stimulating factor 2 (CSF2) expression and enhanced invasion of tumor cells. Together, these results suggest that prior to tumor formation, obesity alters the lung microenvironment, creating niches conducive to metastatic growth. Full article
(This article belongs to the Special Issue Molecular Mechanism of the Interaction Between Cells and Extracellular Matrix in Cancer Progression)
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Review

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17 pages, 6811 KiB  
Review
Matrix Stiffness Contributes to Cancer Progression by Regulating Transcription Factors
by Seiichiro Ishihara and Hisashi Haga
Cancers 2022, 14(4), 1049; https://doi.org/10.3390/cancers14041049 - 18 Feb 2022
Cited by 50 | Viewed by 7314
Abstract
Matrix stiffness is critical for the progression of various types of cancers. In solid cancers such as mammary and pancreatic cancers, tumors often contain abnormally stiff tissues, mainly caused by stiff extracellular matrices due to accumulation, contraction, and crosslinking. Stiff extracellular matrices trigger [...] Read more.
Matrix stiffness is critical for the progression of various types of cancers. In solid cancers such as mammary and pancreatic cancers, tumors often contain abnormally stiff tissues, mainly caused by stiff extracellular matrices due to accumulation, contraction, and crosslinking. Stiff extracellular matrices trigger mechanotransduction, the conversion of mechanical cues such as stiffness of the matrix to biochemical signaling in the cells, and as a result determine the cellular phenotypes of cancer and stromal cells in tumors. Transcription factors are key molecules for these processes, as they respond to matrix stiffness and are crucial for cellular behaviors. The Yes-associated protein (YAP)/transcriptional coactivator with PDZ-binding motif (TAZ) is one of the most studied transcription factors that is regulated by matrix stiffness. The YAP/TAZ are activated by a stiff matrix and promotes malignant phenotypes in cancer and stromal cells, including cancer-associated fibroblasts. In addition, other transcription factors such as β-catenin and nuclear factor kappa B (NF-κB) also play key roles in mechanotransduction in cancer tissues. In this review, the mechanisms of stiffening cancer tissues are introduced, and the transcription factors regulated by matrix stiffness in cancer and stromal cells and their roles in cancer progression are shown. Full article
(This article belongs to the Special Issue Molecular Mechanism of the Interaction Between Cells and Extracellular Matrix in Cancer Progression)
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Other

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12 pages, 17796 KiB  
Perspective
Remodeling the ECM: Implications for Metastasis and Tumor Dormancy
by Julie S. Di Martino, Tasmiah Akhter and Jose Javier Bravo-Cordero
Cancers 2021, 13(19), 4916; https://doi.org/10.3390/cancers13194916 - 30 Sep 2021
Cited by 27 | Viewed by 3367
Abstract
While most primary tumors can be effectively treated, therapeutics fail to efficiently eliminate metastases. Metastases arise from cancer cells that leave the primary tumor and seed distant sites. Recent studies have shown that cancer cells disseminate early during tumor progression and can remain [...] Read more.
While most primary tumors can be effectively treated, therapeutics fail to efficiently eliminate metastases. Metastases arise from cancer cells that leave the primary tumor and seed distant sites. Recent studies have shown that cancer cells disseminate early during tumor progression and can remain dormant for years before they resume growth. In these metastatic organs, cancer cells reside in microenvironments where they interact with other cells, but also with the extracellular matrix (ECM). The ECM was long considered to be an inert, non-cellular component of tissues, providing their architecture. However, in recent years, a growing body of evidence has shown that the ECM is a key driver of cancer progression, and it can exert effects on tumor cells, regulating their metastatic fate. ECM remodeling and degradation is required for the early steps of the metastatic cascade: invasion, tumor intravasation, and extravasation. Similarly, ECM molecules have been shown to be important for metastatic outgrowth. However, the role of ECM molecules on tumor dormancy and their contribution to the dormancy-supportive niches is not well understood. In this perspective article, we will summarize the current knowledge of ECM and its role in tumor metastasis and dormancy. We will discuss how a better understanding of the individual components of the ECM niche and their roles mediating the dormant state of disseminated tumor cells (DTCs) will advance the development of new therapies to target dormant cells and prevent metastasis outgrowth. Full article
(This article belongs to the Special Issue Molecular Mechanism of the Interaction Between Cells and Extracellular Matrix in Cancer Progression)
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