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Cancers
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Communication and Accessibility in the Tumor Microenvironment as a Therapeutic...
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Communication and Accessibility in the Tumor Microenvironment as a Therapeutic Target

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

Deadline for manuscript submissions: 20 December 2024 | Viewed by 4465

Special Issue Editors

Dr. Gema Jiménez-González

E-Mail Website
Guest Editor
Instituto de Investigación Biosanitaria de Granada (ibs.GRANADA), Centre for Biomedical Research, University of Granada, E-18016 Granada, Spain
Interests: 3D bioprinting; bioinks; hydrogels; pathological processes; cancer; cancer stem cells; tumor microenvironment; organoids; cancer diagnosis; cancer treatment; translational research; personalized medicine; tumor-on-a-chip; metastasis-on-a-chip; organ-on-a-chip
Dr. Carmen Griñán-Lisón

E-Mail Website
Guest Editor
Instituto de Investigación Biosanitaria de Granada (ibs.GRANADA), Centre for Biomedical Research, University of Granada, E-18016 Granada, Spain
Interests: organoids; pathological processes; cancer; cancer stem cells; tumor microenvironment; cancer diagnosis; cancer treatment; translational research; personalized medicine; tumor-on-a-chip; metastasis-on-a-chip; organ-on-a-chip; 3D bioprinting; bioinks; hydrogels

Special Issue Information

Dear Colleagues,

The tumor microenvironment (TME) is a key factor that orchestrates tumor processes in different ways. The TME is constituted of cellular components comprising cancer stem cells and differentiated cancer cells, as well as stromal cells as mesenchymal stem cells, cancer-associated fibroblasts, endothelial cells, and immune system cells. There has been a tendency to simplify the TME to these aforementioned cellular components, but it also includes a complex and dynamic cellular communication network consisting of cytokines, growth factors, extracellular vesicles, miRNAs, among others, and an all-encompassing extracellular matrix (ECM). Currently, cancer therapies are advancing and are not exclusively directed at a single cell type, but rather target the entire TME complex, including cellular communication and the ECM that supports it.

This Special Issue aims to highlight the role of tumor communication and the ECM in treatment resistance, as well as being the objects of new targeted therapies. We are pleased to include original articles and reviews in this Special Issue.

Dr. Gema Jiménez-González
Dr. Carmen Griñán-Lisón
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

  • tumor microenvironment
  • cellular communication
  • tumor secretome
  • signaling
  • extracellular matrix
  • cancer treatment
  • targeted treatment

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Published Papers (2 papers)

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Research

16 pages, 2819 KiB  
Article
Paracrine Activation of STAT3 Drives GM-CSF Expression in Breast Carcinoma Cells, Generating a Symbiotic Signaling Network with Breast Carcinoma-Associated Fibroblasts
by Kingsley O. Osuala, Anita Chalasani, Neha Aggarwal, Kyungmin Ji and Kamiar Moin
Cancers 2024, 16(16), 2910; https://doi.org/10.3390/cancers16162910 - 22 Aug 2024
Viewed by 584
Abstract
This study evaluated the paracrine signaling between breast carcinoma-associated fibroblasts (CAFs) and breast cancer (BCa) cells. Resolving cell–cell communication in the BCa tumor microenvironment (TME) will aid the development of new therapeutics. Here, we utilized our patented TAME (tissue architecture and microenvironment engineering) [...] Read more.
This study evaluated the paracrine signaling between breast carcinoma-associated fibroblasts (CAFs) and breast cancer (BCa) cells. Resolving cell–cell communication in the BCa tumor microenvironment (TME) will aid the development of new therapeutics. Here, we utilized our patented TAME (tissue architecture and microenvironment engineering) 3D culture microphysiological system, which is a suitable pathomimetic avatar for the study of the BCa TME. We cultured in 3D BCa cells and CAFs either alone or together in cocultures and found that when cocultured, CAFs enhanced the invasive characteristics of tumor cells, as shown by increased proliferation and spread of tumor cells into the surrounding matrix. Secretome analysis from 3D cultures revealed a relatively high secretion of IL-6 by CAFs. A marked increase in the secretion of granulocyte macrophage-colony stimulating factor (GM-CSF) when carcinoma cells and CAFs were in coculture was also observed. We theorized that the CAF-secreted IL-6 functions in a paracrine manner to induce GM-CSF expression and secretion from carcinoma cells. This was confirmed by evaluating the activation of STAT3 and gene expression of GM-CSF in carcinoma cells exposed to CAF-conditioned media (CAF-CM). In addition, the treatment of CAFs with BCa cell-CM yielded a brief upregulation of GM-CSF followed by a marked decrease, indicating a tightly regulated control of GM-CSF in CAFs. Secretion of IL-6 from CAFs drives the activation of STAT3 in BCa cells, which in turn drives the expression and secretion of GM-CSF. As a result, CAFs exposed to BCa cell-secreted GM-CSF upregulate inflammation-associated genes such as IL-6, IL-6R and IL-8, thereby forming a positive feedback loop. We propose that the tight regulation of GM-CSF in CAFs may be a novel regulatory pathway to target for disrupting the CAF:BCa cell symbiotic relationship. These data provide yet another piece of the cell–cell communication network governing the BCa TME. Full article
(This article belongs to the Special Issue Communication and Accessibility in the Tumor Microenvironment as a Therapeutic Target)
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14 pages, 3176 KiB  
Article
A Fibroblast-Derived Secretome Stimulates the Growth and Invasiveness of 3D Plexiform Neurofibroma Spheroids
by Kyungmin Ji, George J. Schwenkel, Raymond R. Mattingly, Harini G. Sundararaghavan, Zheng Gang Zhang and Michael Chopp
Cancers 2024, 16(14), 2498; https://doi.org/10.3390/cancers16142498 - 9 Jul 2024
Viewed by 3407
Abstract
Plexiform neurofibromas (PNs) occur in about a half of neurofibromatosis type 1 (NF1) patients and have garnered significant research attention due to their capacity for growth and potential for malignant transformation. NF1 plexiform neurofibroma (pNF1) is a complex tumor composed of Schwann cell-derived [...] Read more.
Plexiform neurofibromas (PNs) occur in about a half of neurofibromatosis type 1 (NF1) patients and have garnered significant research attention due to their capacity for growth and potential for malignant transformation. NF1 plexiform neurofibroma (pNF1) is a complex tumor composed of Schwann cell-derived tumor cells (Nf1−/−) and the tumor microenvironment (TME). Although it has been widely demonstrated that the TME is involved in the formation of neurofibromas, little is known about the effects of the TME on the subsequent progression of human pNF1. Elucidating the molecular interactions between tumor cells and the TME may provide new therapeutic targets to reduce the progression of pNF1. In the present study, we focused on the contributions of fibroblasts, the most abundant cell types in the TME, to the growth of pNF1. To simulate the TME, we used a three-dimensional (3D) coculture model of immortalized pNF1 tumor cells (Nf1−/−) and primary fibroblasts (Nf1+/−) derived from pNF1 patients. We performed live-cell imaging of 3D/4D (3D in real-time) cultures through confocal microscopy followed by 3D quantitative analyses using advanced imaging software. The growth of pNF1 spheroids in 3D cocultures with fibroblasts was significantly greater than that of pNF1 spheroids in 3D monocultures. An increase in the growth of pNF1 spheroids also occurred when they were cultured with conditioned media (CM) from fibroblasts. Moreover, fibroblast-derived CM increased the invasive outgrowth and further local invasion of pNF1 spheroids. Interestingly, when small extracellular vesicles (sEVs) were depleted from the fibroblast-derived CM, the stimulation of the growth of pNF1 spheroids was lost. Our results suggest that fibroblast-derived sEVs are a therapeutic target for reducing the growth of pNF1. Full article
(This article belongs to the Special Issue Communication and Accessibility in the Tumor Microenvironment as a Therapeutic Target)
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