ijms-logo

Journal Browser

Journal Browser

Radiation and Tumor Microenvironment: Looking for Radio-Transmitted Signals

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: closed (10 August 2020) | Viewed by 4652

Special Issue Editor

BioScience Laboratory, IRCCS Istituto Romagnolo per lo Studio dei Tumori (IRST) “Dino Amadori”, 47014 Meldola, Italy
Interests: radiobiology; drug discovery; stem cell; anticancer drugs; targeted therapy; cancer drug resistance; 3D in vitro models; in vivo models; oncology

Special Issue Information

Dear Colleagues,

Radiotherapy (RT) is known to be a pivotal treatment for early and metastatic cancer. In addition to inducing lethal DNA damage in tumor and stromal cells, RT can alter the interactions between tumor cells and the different components of the tumor microenvironment (TME), including endothelial cells, fibroblasts, immune cells, extracellular components (cytokines, soluble factors, the extracellular matrix), and the complex vascular network. Extracellular vesicles (EVs) represent an additional means of communication between all of these actors, conveying several biomacromolecular complexes that are constituted by RNA, DNA, proteins, microRNAs, etc. Currently, it is commonly believed that the TME plays a key role in the modulation of the RT response and in clinical outcome and that RT in combination with immunotherapy may lead to the activation of an immune response and to the switching of the TME from immunosuppressive to immunoreactive.  An example of the interaction between the TME and RT is represented by the abscopal effect, in which focal radiation can result in out-of-field responses.

For these reasons, exploring the relatonship between RT and cell–cell comunication in the TME could be crucial to improving radiotherapy outcomes and at the same time discovering predictive radiotherapy biomarkers.

This Special Issue, entitled “Radiation and Tumor Microenvironment: Looking for Radio-Transmitted Signals”, will cover a selection of recent research topics and current review articles in the field of Radiobiology and the TME. Experimental papers, up-to-date review articles, and commentaries are all welcome.

Dr. Anna Tesei
Guest Editor

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • radiotherapy
  • cancer
  • tumor microenvironment
  • immunosuppressive mileu
  • inflammation
  • extracellular vesicles
  • radiotherapy resistance.

Published Papers (2 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

17 pages, 2247 KiB  
Article
Investigating the Benefit of Combined Androgen Modulation and Hypofractionation in Prostate Cancer
by Alice Zamagni, Michele Zanoni, Michela Cortesi, Chiara Arienti, Sara Pignatta, Antonella Naldini, Anna Sarnelli, Antonino Romeo and Anna Tesei
Int. J. Mol. Sci. 2020, 21(22), 8447; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21228447 - 10 Nov 2020
Viewed by 1697
Abstract
Hypofractionation is currently considered a valid alternative to conventional radiotherapy for the treatment of patients with organ-confined prostate cancer. Recent data have demonstrated that extreme hypofractionation, which involves the use of a high radiation dose per delivered fraction and concomitant reduction of sessions, [...] Read more.
Hypofractionation is currently considered a valid alternative to conventional radiotherapy for the treatment of patients with organ-confined prostate cancer. Recent data have demonstrated that extreme hypofractionation, which involves the use of a high radiation dose per delivered fraction and concomitant reduction of sessions, is a safe and effective treatment, even though its radiobiological rationale is still lacking. The present work aims to investigate the biological basis sustaining this approach and to evaluate the potential of a hypofractionated regimen in combination with androgen deprivation therapy, one of the major standards of care for prostate cancer. Findings show that androgen receptor (AR) modulation, by use of androgens and antiandrogens, has a significant impact on cell survival, especially in hypoxic conditions (4% O2). Subsequent experiments have revealed that AR activity as a transcription factor is involved in the onset of malignant senescence-associated secretory phenotype (SASP) and activation of DNA repair cascade. In particular, we found that AR stimulation in hypoxic conditions promotes the enhanced transcription of ATM gene, the cornerstone kinase of the DNA damage repair genes. Together, these data provide new potential insights to justify the use of androgen deprivation therapy, in particular with second-generation anti-androgens such as enzalutamide, in combination with radiotherapy. Full article
Show Figures

Figure 1

16 pages, 4251 KiB  
Article
RIP1 Is a Novel Component of γ-ionizing Radiation-Induced Invasion of Non-Small Cell Lung Cancer Cells
by A-Ram Kang, Jeong Hyun Cho, Na-Gyeong Lee, Jie-Young Song, Sang-Gu Hwang, Dae-Hee Lee, Hong-Duck Um and Jong Kuk Park
Int. J. Mol. Sci. 2020, 21(13), 4584; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21134584 - 28 Jun 2020
Cited by 7 | Viewed by 2623
Abstract
Previously, we demonstrated that γ-ionizing radiation (IR) triggers the invasion/migration of A549 cells via activation of an EGFR–p38/ERK–STAT3/CREB-1–EMT pathway. Here, we have demonstrated the involvement of a novel intracellular signaling mechanism in γ-ionizing radiation (IR)-induced migration/invasion. Expression of receptor-interacting protein (RIP) 1 was [...] Read more.
Previously, we demonstrated that γ-ionizing radiation (IR) triggers the invasion/migration of A549 cells via activation of an EGFR–p38/ERK–STAT3/CREB-1–EMT pathway. Here, we have demonstrated the involvement of a novel intracellular signaling mechanism in γ-ionizing radiation (IR)-induced migration/invasion. Expression of receptor-interacting protein (RIP) 1 was initially increased upon exposure of A549, a non-small cell lung cancer (NSCLC) cell line, to IR. IR-induced RIP1 is located downstream of EGFR and involved in the expression/activity of matrix metalloproteases (MMP-2 and MMP-9) and vimentin, suggesting a role in epithelial-mesenchymal transition (EMT). Our experiments showed that IR-induced RIP1 sequentially induces Src-STAT3-EMT to promote invasion/migration. Inhibition of RIP1 kinase activity and expression blocked induction of EMT by IR and suppressed the levels and activities of MMP-2, MMP-9 and vimentin. IR-induced RIP1 activation was additionally associated with stimulation of the transcriptional factor NF-κB. Specifically, exposure to IR triggered NF-κB activation and inhibition of NF-κB suppressed IR-induced RIP1 expression, followed by a decrease in invasion/migration as well as EMT. Based on the collective results, we propose that IR concomitantly activates EGFR and NF-κB and subsequently triggers the RIP1–Src/STAT3–EMT pathway, ultimately promoting metastasis. Full article
Show Figures

Figure 1

Back to TopTop