ijms-logo

Journal Browser

Journal Browser

Special Issue "Tumor Microenvironment 3.0"

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

Deadline for manuscript submissions: 20 March 2020.

Special Issue Editor

Prof. Dr. Naofumi Mukaida
E-Mail Website1 Website2
Guest Editor
Kanazawa University, Division of Molecular Bioregulation, Kanazawa, Japan
Interests: chemokine; tumor microenvironment; metastasis; invasion; Immunology; Laboratory medicine; Experimental Pathology; Pathological Medical Biochemistry
Special Issues and Collections in MDPI journals

Special Issue Information

Dear Colleagues,

The accumulation of gene mutations can transform normal cells into cancer cells, which are required, but not sufficient, to induce cancer tissues. Cancer development and its malignant progression unexceptionally proceeds under the influence of tumor microenvironments, which are governed by the communication between cancer cells and normal resident cells present in tumor tissues, such as leukocytes, endothelial cells, and fibroblasts. Moreover, normal cells present in tumor tissues frequently support the survival of cancer stem cells by providing them with niche, thereby inducing resistance to chemotherapy and radiotherapy. Thus, in order to identify druggable targets for exploiting efficient anti-cancer strategies, it is mandatory to clarify the interplay of cancer cells with intratumoral normal cells at molecular levels. Here, in this Special Issue “Tumor Microenvironments”, we will discuss various types of mediators including cytokines, chemokines, extracellular vesicles, and lipid mediators, which are deeply involved in the interaction between cancer cells and normal cells in cancer tissues.

Prof. Dr. Naofumi Mukaida
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 papers will be 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

  • angiogenesis
  • chemokine
  • cytokine
  • endothelial cell
  • fibroblast
  • invasion
  • lipid mediator
  • leukocyte
  • metastasis
  • niche

Related Special Issues

Published Papers (1 paper)

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

Research

Open AccessArticle
Cancer Cell-Derived Granulocyte-Macrophage Colony-Stimulating Factor Is Dispensable for the Progression of 4T1 Murine Breast Cancer
Int. J. Mol. Sci. 2019, 20(24), 6342; https://doi.org/10.3390/ijms20246342 - 16 Dec 2019
Abstract
We previously reported that 4T1 murine breast cancer cells produce GM-CSF that up-regulates macrophage expression of several cancer promoting genes, including Mcp-1/Ccl2, Ccl17 and Rankl, suggesting a critical role of cancer cell-derived GM-CSF in cancer progression. Here, we attempted to define [...] Read more.
We previously reported that 4T1 murine breast cancer cells produce GM-CSF that up-regulates macrophage expression of several cancer promoting genes, including Mcp-1/Ccl2, Ccl17 and Rankl, suggesting a critical role of cancer cell-derived GM-CSF in cancer progression. Here, we attempted to define whether 4T1 cell-derived GM-CSF contributes to the expression of these genes by 4T1tumors, and their subsequent progression. Intraperitoneal injection of anti-GM-CSF neutralizing antibody did not decrease the expression of Mcp-1, Ccl17 or Rankl mRNA by 4T1 tumors. To further examine the role of cancer cell-derived GM-CSF, we generated GM-CSF-deficient 4T1 cells by using the Crisper-Cas9 system. As previously demonstrated, 4T1 cells are a mixture of cells and cloning of cells by itself significantly reduced tumor growth and lung metastasis. By contrast, GM-CSF-deficiency did not affect tumor growth, lung metastasis or the expression of these chemokine and cytokine genes in tumor tissues. By in-situ hybridization, the expression of Mcp-1 mRNA was detected in both F4/80-expressing and non-expressing cells in tumors of GM-CSF-deficient cells. These results indicate that cancer cell-derived GM-CSF is dispensable for the tuning of the 4T1 tumor microenvironment and the production of MCP-1, CCL17 or RANKL in the 4T1 tumor microenvironment is likely regulated by redundant mechanisms. Full article
(This article belongs to the Special Issue Tumor Microenvironment 3.0)
Show Figures

Figure 1

Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

 
Back to TopTop