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Cell–Microenvironment Crosstalk, Models, and Molecular Mechanisms in Rhabdomyosarcoma: Current and...
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Cell–Microenvironment Crosstalk, Models, and Molecular Mechanisms in Rhabdomyosarcoma: Current and Future Perspectives

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Microenvironment".

Deadline for manuscript submissions: closed (20 May 2022) | Viewed by 7194

Special Issue Editors

Dr. Michela Pozzobon

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Guest Editor
Stem Cells and Regenerative Medicine Lab, Institute of Pediatric Research Città Della Speranza, University of Padova, Padova, Italy
Interests: muscle reconstruction; extracellular vesicles in regenerative medicine; rhabdomyosarcoma microenvironment
Special Issues, Collections and Topics in MDPI journals
Dr. Silvia Codenotti

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Guest Editor
Department of Molecular and Translational Medicine (DMMT), University of Brescia, Brescia, Italy
Interests: rhabdomyosarcoma
Special Issues, Collections and Topics in MDPI journals
Dr. Claudia Fuoco

E-Mail Website
Guest Editor
Dipartimento di Biologia, Università degli Studi di Roma Tor Vergata, Rome, Italy
Interests: cell heterogeneity; mass cytometry; skeletal muscle tissue engineering; skeletal muscle regeneration and pathogenesis
Special Issues, Collections and Topics in MDPI journals
Dr. Alessandro Fanzani

E-Mail Website
Guest Editor
Department of Molecular and Translational Medicine (DMMT), University of Brescia, Viale Europa 11, 25123 Brescia, Italy
Interests: rhabdomyosarcoma; caveolins; cavins; oxidative stress; muscle
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

It is with great pleasure and enthusiasm that we present to you this Special Issue of Medical Sciences. This issue aims at investigating the latest aspects under study to unveil the complexity of Rhabdomyosarcoma. The prognosis of this pediatric disease has improved significantly in recent years, but the outcome of patients with metastatic or refractory RMS remains dismal. Therefore, new treatment options targeting both malignant tumors and the context in which they live are paramount. Malignant cells do not act alone in cancer progression but need enduring interactions and crosstalk with supporting cell types and extracellular matrix components (ECM) that form the tumor microenvironment. The former includes cancer-associated fibroblasts (CAFs), myofibroblasts, and other cells, generally known as stromal cells. Generally, in tumors, CAFs exhibit enhanced proliferation and are responsible for the production and deposition of soluble and insoluble extracellular matrix molecules, such as collagens, structural proteoglycans, proteolytic enzymes, and growth factors. Soluble molecules present in close proximity to tumor cells bind to membrane receptors and initiate intracellular signaling cascades necessary to sustain proliferation, angiogenesis, and initiation of invasion and metastasis.

In this view, the present Special Issue aims to collect new aspects that are under exploration on the rhabdomyosarcoma microenvironment and tumor progression, considering the following aspects:

  1. The microenvironment;
  2. The immunoenvironment;
  3. Extracellular vesicles;
  4. Models to study rhabdomyosarcoma progression.

We look forward to receiving your contributions summarizing or explaining your research to this Special Issue.

Dr. Michela Pozzobon
Dr. Silvia Codenotti
Dr. Claudia Fuoco
Dr. Alessandro Fanzani
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. Cells 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 2700 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

  • rhabdomyosarcoma
  • microenvironment
  • cancer cells
  • extracellular vesicles

Related Special Issue

Published Papers (2 papers)

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Research

19 pages, 4014 KiB  
Article
Hyperactive Akt1 Signaling Increases Tumor Progression and DNA Repair in Embryonal Rhabdomyosarcoma RD Line and Confers Susceptibility to Glycolysis and Mevalonate Pathway Inhibitors
by Silvia Codenotti, Daniela Zizioli, Luca Mignani, Sara Rezzola, Giovanna Tabellini, Silvia Parolini, Arianna Giacomini, Michela Asperti, Maura Poli, Delia Mandracchia, Marika Vezzoli, Simona Bernardi, Domenico Russo, Stefania Mitola, Eugenio Monti, Luca Triggiani, Davide Tomasini, Stefano Gastaldello, Matteo Cassandri, Rossella Rota, Francesco Marampon and Alessandro Fanzaniadd Show full author list remove Hide full author list
Cells 2022, 11(18), 2859; https://doi.org/10.3390/cells11182859 - 14 Sep 2022
Cited by 5 | Viewed by 4106
Abstract
In pediatric rhabdomyosarcoma (RMS), elevated Akt signaling is associated with increased malignancy. Here, we report that expression of a constitutively active, myristoylated form of Akt1 (myrAkt1) in human RMS RD cells led to hyperactivation of the mammalian target of rapamycin (mTOR)/70-kDa ribosomal protein [...] Read more.
In pediatric rhabdomyosarcoma (RMS), elevated Akt signaling is associated with increased malignancy. Here, we report that expression of a constitutively active, myristoylated form of Akt1 (myrAkt1) in human RMS RD cells led to hyperactivation of the mammalian target of rapamycin (mTOR)/70-kDa ribosomal protein S6 kinase (p70S6K) pathway, resulting in the loss of both MyoD and myogenic capacity, and an increase of Ki67 expression due to high cell mitosis. MyrAkt1 signaling increased migratory and invasive cell traits, as detected by wound healing, zymography, and xenograft zebrafish assays, and promoted repair of DNA damage after radiotherapy and doxorubicin treatments, as revealed by nuclear detection of phosphorylated H2A histone family member X (γH2AX) through activation of DNA-dependent protein kinase (DNA-PK). Treatment with synthetic inhibitors of phosphatidylinositol-3-kinase (PI3K) and Akt was sufficient to completely revert the aggressive cell phenotype, while the mTOR inhibitor rapamycin failed to block cell dissemination. Furthermore, we found that pronounced Akt1 signaling increased the susceptibility to cell apoptosis after treatments with 2-deoxy-D-glucose (2-DG) and lovastatin, enzymatic inhibitors of hexokinase, and 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase (HMGCR), especially in combination with radiotherapy and doxorubicin. In conclusion, these data suggest that restriction of glucose metabolism and the mevalonate pathway, in combination with standard therapy, may increase therapy success in RMS tumors characterized by a dysregulated Akt signaling. Full article
(This article belongs to the Special Issue Cell–Microenvironment Crosstalk, Models, and Molecular Mechanisms in Rhabdomyosarcoma: Current and Future Perspectives)
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17 pages, 4262 KiB  
Article
CD147 Promotes Tumorigenesis via Exosome-Mediated Signaling in Rhabdomyosarcoma
by Assil Fahs, Nader Hussein, Hasan Zalzali, Farah Ramadan, Farah Ghamloush, Hani Tamim, Mahmoud El Homsi, Bassam Badran, Fouad Boulos, Ayman Tawil, Sandra E. Ghayad and Raya Saab
Cells 2022, 11(15), 2267; https://doi.org/10.3390/cells11152267 - 22 Jul 2022
Cited by 3 | Viewed by 2656
Abstract
Rhabdomyosarcoma (RMS) is an aggressive childhood soft-tissue tumor, with propensity for local invasion and distant metastasis. Exosomes are secreted vesicles that mediate paracrine signaling by delivering functional proteins and miRNA to recipient cells. The transmembrane protein CD147, also known as Basigin or EMMPRIN, [...] Read more.
Rhabdomyosarcoma (RMS) is an aggressive childhood soft-tissue tumor, with propensity for local invasion and distant metastasis. Exosomes are secreted vesicles that mediate paracrine signaling by delivering functional proteins and miRNA to recipient cells. The transmembrane protein CD147, also known as Basigin or EMMPRIN, is enriched in various tumor cells, as well as in tumor-derived exosomes, and has been correlated with poor prognosis in several types of cancer, but has not been previously investigated in RMS. We investigated the effects of CD147 on RMS cell biology and paracrine signaling, specifically its contribution to invasion and metastatic phenotype. CD147 downregulation diminishes RMS cell invasion and inhibits anchorage-independent growth in vitro. While treatment of normal fibroblasts with RMS-derived exosomes results in a significant increase in proliferation, migration, and invasion, these effects are reversed when using exosomes from CD147-downregulated RMS cells. In human RMS tissue, CD147 was expressed exclusively in metastatic tumors. Altogether, our results demonstrate that CD147 contributes to RMS tumor cell aggressiveness, and is involved in modulating the microenvironment through RMS-secreted exosomes. Targeted inhibition of CD147 reduces its expression levels within the isolated exosomes and reduces the capacity of these exosomes to enhance cellular invasive properties. Full article
(This article belongs to the Special Issue Cell–Microenvironment Crosstalk, Models, and Molecular Mechanisms in Rhabdomyosarcoma: Current and Future Perspectives)
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