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Cells
Special Issues
Cell–Cell Interactome-Based Therapies for Osteosarcoma
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Cell–Cell Interactome-Based Therapies for Osteosarcoma

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

Deadline for manuscript submissions: 31 December 2024 | Viewed by 2114

Special Issue Editors

Dr. Frédéric Lézot

E-Mail Website
Guest Editor
Sorbone Université, INSERM UMR933, Hôpital Armand Trousseau (AP-HP), F-75012 Paris, France
Interests: skeleton growth defects; primary bone tumors; bone microenvironment; pathophysiology
Special Issues, Collections and Topics in MDPI journals
Dr. Javier Munoz

E-Mail Website
Guest Editor
Institut de Cancérologie de l'Ouest, Tumor Heterogeneity and Precision Medicine Laboratory, 44805 Saint-Herblain, France
Interests: osteosarcoma; tumor heterogeneity; tumor microenvironment; cell signaling pathway; 3D culture; microfluidics; bone remodeling; drug screening

Special Issue Information

Dear Colleagues,

The therapeutic protocols currently used to treat osteosarcoma are limited in two non-exclusive situations: resistance to chemotherapy agents and the occurrence of metastases. During recent years, researchers have focused their efforts to reduce the occurrence of these situations. For both deleterious events, the qualitative and quantitative composition of cells, as fibroblastic cells (CAF), immune cells (TIL, TAM), endothelial cells and stromal cells, in the tumor microenvironment, as well as the cell–cell interactions have been shown to play a key role. Similarly, the ability of tumor cells to hijack interactions with some of these cells, for example by luring the immune system through the expression of immune checkpoints, is a major factor of poor prognostics, linked to tumor escape.

As such, we are pleased to introduce this Special Issue dedicated to publishing original articles and reviews on all aspects associated to the role of cell–cell interactions in the resistance to treatment and metastatic dissemination of osteosarcoma, which will increase our knowledge in those fields and open therapeutic avenues for the future.

Dr. Frédéric Lézot
Dr. Javier Munoz
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

  • osteosarcoma
  • cell–cell interactions
  • microenvironment
  • metastases
  • resistance
  • chemotherapy
  • immune checkpoints

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Published Papers (2 papers)

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12 pages, 2735 KiB  
Article
CD47 in Osteosarcoma: Correlation with Metastasis and Macrophage-Mediated Phagocytosis
by Yunmi Ko, Seog-Yun Park, Jong Woong Park, June Hyuk Kim, Hyun Guy Kang and Jun Ah Lee
Cells 2024, 13(22), 1862; https://doi.org/10.3390/cells13221862 - 10 Nov 2024
Viewed by 634
Abstract
CD47 is expressed on cell surfaces and acts as a “don’t eat me” signal by interacting with signal-regulatory protein-α on the macrophage surface. Some cancer cells express CD47 protein and can evade macrophage phagocytosis. Herein, we evaluated the feasibility of targeting CD47 for [...] Read more.
CD47 is expressed on cell surfaces and acts as a “don’t eat me” signal by interacting with signal-regulatory protein-α on the macrophage surface. Some cancer cells express CD47 protein and can evade macrophage phagocytosis. Herein, we evaluated the feasibility of targeting CD47 for osteosarcoma by analyzing its expression patterns, clinicopathological correlations, and immunotherapeutic potential. We performed a retrospective analysis on 24 biopsy samples from patients with osteosarcoma to investigate correlations between CD47 protein positivity and clinicopathological characteristics. CD47 protein expression was detected in 20.8% of the biopsy samples. CD47 positivity correlated with metastasis at diagnosis. Patients with CD47-positive tumors were older than those with CD47-negative tumors. However, CD47 protein expression was not associated with sex, tumor size, or histologic response to preoperative chemotherapy. In vitro, CD47 antibody (B6H12) did not affect osteosarcoma cell viability or apoptosis. In a wound-healing assay, CD47 inhibited the migration of osteosarcoma cells. Differentiated macrophages exhibited higher phagocytic activity against osteosarcoma cells when pretreated with B6H12 compared with the isotype control. Our preliminary data suggest a possible interaction between CD47 protein and macrophage phagocytosis in osteosarcoma metastasis. A better understanding of the role of CD47 is necessary to develop an innovative immunotherapeutic approach against osteosarcoma. Full article
(This article belongs to the Special Issue Cell–Cell Interactome-Based Therapies for Osteosarcoma)
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17 pages, 7808 KiB  
Article
PAK4 Is Involved in the Stabilization of PD-L1 and the Resistance to Doxorubicin in Osteosarcoma and Predicts the Survival of Diagnosed Patients
by Junyue Zhang, Yiping Song, Ae-Ri Ahn, Ho Sung Park, See-Hyoung Park, Young Jae Moon, Kyoung Min Kim and Kyu Yun Jang
Cells 2024, 13(17), 1444; https://doi.org/10.3390/cells13171444 - 28 Aug 2024
Viewed by 1193
Abstract
PAK4 and PD-L1 have been suggested as novel therapeutic targets in human cancers. Moreover, PAK4 has been suggested to be a molecule closely related to the immune evasion of cancers. Therefore, this study evaluated the roles of PAK4 and PD-L1 in the progression [...] Read more.
PAK4 and PD-L1 have been suggested as novel therapeutic targets in human cancers. Moreover, PAK4 has been suggested to be a molecule closely related to the immune evasion of cancers. Therefore, this study evaluated the roles of PAK4 and PD-L1 in the progression of osteosarcomas in 32 osteosarcomas and osteosarcoma cells. In human osteosarcomas, immunohistochemical positivity for the expression of PAK4 (overall survival, p = 0.028) and PD-L1 (relapse-free survival, p = 0.002) were independent indicators for the survival of patients in a multivariate analysis. In osteosarcoma cells, the overexpression of PAK4 increased proliferation and invasiveness, while the knockdown of PAK4 suppressed proliferation and invasiveness. The expression of PAK4 was associated with the expression of the molecules related to cell cycle regulation, invasion, and apoptosis. PAK4 was involved in resistance to apoptosis under a treatment regime with doxorubicin for osteosarcoma. In U2OS cells, PAK4 was involved in the stabilization of PD-L1 from ubiquitin-mediated proteasomal degradation and the in vivo infiltration of immune cells such as regulatory T cells and PD1-, CD4-, and CD8-positive cells in mice tumors. In conclusion, this study suggests that PAK4 is involved in the progression of osteosarcoma by promoting proliferation, invasion, and resistance to doxorubicin and stabilized PD-L1 from proteasomal degradation. Full article
(This article belongs to the Special Issue Cell–Cell Interactome-Based Therapies for Osteosarcoma)
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