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Signaling Pathways between Cancer and Immune Cells
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Signaling Pathways between Cancer and Immune Cells

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 (20 September 2021) | Viewed by 12279

Special Issue Editor

Dr. Anuraag Shrivastav

E-Mail Website
Guest Editor
Department of Biology, The University of Winnipeg, Winnipeg, MB R3B 2G3, Canada
Interests: cancer biomarkers; cancer signaling; metastases; immunomodulation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Despite the consistent advancement in cancer diagnosis and treatment, cancer remains the second leading cause of death globally, accounting for one in six deaths. The immune system plays a vital role in the onset and progression of cancer, and the immune response to cancer can be innate or adaptive. Therefore, immune manipulation for cancer treatment is emerging as an effective therapeutic strategy. Recent advancements, including successful therapies targeting program cell death protein-1 (PD1) expressed in immune cells or programmed death-ligand 1 (PD-L1) expressed in cancer cells, are a testament to the effectiveness of immune regulation in cancer treatment. The intercellular communication between cancer cells and immune cells is well established. The intercellular communications between cancer and immune cells are regulated by myriad signaling pathways activated in cancer cells, resulting in perturbation of signaling pathways in immune cells. This Special Issue focuses on bringing together research focused on understanding signaling pathways between cancer and immune cells that would provide more in-depth insight into cancer onset and progression.

This Special Issue invites research articles on the basic, translational, or clinical aspects of signaling pathways between cancer and immune cells to provide a comprehensive understanding of cancer.

Dr. Anuraag Shrivastav
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

  • Cancer signaling
  • Intercellular signaling
  • T cell signalling
  • Grwoth factors signalling pathways
  • PD1
  • PD-L1
  • Apoptosis
  • Immune surveilance pathways in cancer

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Published Papers (3 papers)

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Research

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18 pages, 4233 KiB  
Article
Withholding of M-CSF Supplement Reprograms Macrophages to M2-Like via Endogenous CSF-1 Activation
by Yu-Chih Chen, Yin-Siew Lai, Yan-Der Hsuuw and Ko-Tung Chang
Int. J. Mol. Sci. 2021, 22(7), 3532; https://doi.org/10.3390/ijms22073532 - 29 Mar 2021
Cited by 22 | Viewed by 4737
Abstract
Macrophage colony-stimulating factor (M-CSF or CSF-1) is known to have a broad range of actions on myeloid cells maturation, including the regulation of macrophage differentiation, proliferation and survival. Macrophages generated by M-CSF stimulus have been proposed to be alternatively activated or M2 phenotype. [...] Read more.
Macrophage colony-stimulating factor (M-CSF or CSF-1) is known to have a broad range of actions on myeloid cells maturation, including the regulation of macrophage differentiation, proliferation and survival. Macrophages generated by M-CSF stimulus have been proposed to be alternatively activated or M2 phenotype. M-CSF is commonly overexpressed by tumors and is also known to enhance tumor growth and aggressiveness via stimulating pro-tumor activities of tumor-associated macrophages (TAMs). Currently, inhibition of CSF-1/CSF-1R interaction by therapeutic antibody to deplete TAMs and their pro-tumor functions is becoming a prevalent strategy in cancer therapy. However, its antitumor activity shows a limited single-agent effect. Therefore, macrophages in response to M-CSF interruption are pending for further investigation. To achieve this study, bone marrow derived macrophages were generated in vitro by M-CSF stimulation for 7 days and then continuously grown until day 21 in M-CSF absence. A selective pressure for cell survival was initiated after withdrawal of M-CSF. The surviving cells were more prone to M2-like phenotype, even after receiving interleukin-4 (IL-4) stimulation. The transcriptome analysis unveiled that endogenous CSF-1 level was dramatically up-regulated and numerous genes downstream to CSF-1 covering tumor necrosis factor (TNF), ras-related protein 1 (Rap1) and phosphatidylinositol 3-kinase (PI3K)-protein kinase B (AKT) signaling pathway were significantly modulated, especially for proliferation, migration and adhesion. Moreover, the phenomenal increase of miR-21-5p and genes related to pro-tumor activity were observed in parallel. In summary, withholding of CSF-1/CSF-1R interaction would rather augment than suspend the M-CSF-driven pro-tumor activities of M2 macrophages in a long run. Full article
(This article belongs to the Special Issue Signaling Pathways between Cancer and Immune Cells)
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11 pages, 1054 KiB  
Article
Insulin-Like Growth Factor Binding Protein-3 Binds to Histone 3
by Apurva Bhardwaj, Kumar Alok Pathak, Anuraag Shrivastav and Shailly Varma Shrivastav
Int. J. Mol. Sci. 2021, 22(1), 407; https://doi.org/10.3390/ijms22010407 - 2 Jan 2021
Cited by 6 | Viewed by 3223
Abstract
Insulin-like growth factor (IGF) binding protein-3 (IGFBP-3) is an essential protein that regulates cellular processes such as cell proliferation, apoptosis, and differentiation. It is known to bind with several proteins to carry out various cellular functions. In this study, we report for the [...] Read more.
Insulin-like growth factor (IGF) binding protein-3 (IGFBP-3) is an essential protein that regulates cellular processes such as cell proliferation, apoptosis, and differentiation. It is known to bind with several proteins to carry out various cellular functions. In this study, we report for the first time that IGFBP-3 is a histone 3 (H3) binding protein. Sub-cellular fractionation was performed to separate into cytosolic fraction, nucleic acid binding protein fraction and insoluble nuclear fraction. Using ligand blot analysis, we identified a ~15 kDa protein that can interact with IGFBP-3 in the insoluble nuclear fraction. The 15 kDa protein was confirmed as histone 3 by far-Western blot analysis and co-immunoprecipitation experiments. A dot-blot experiment further validated the binding of IGFBP-3 with H3. The intensity of IGFBP-3 on dot-blot showed a proportional increase with H3 concentrations between 2.33 pmol–37.42 pmol. Our results support the presence of protein-protein interaction between IGFBP-3 and H3. The physical binding between IGFBP-3 and H3 could indicate its yet another cellular role in regulating the chromatin remodeling for gene transcription. Full article
(This article belongs to the Special Issue Signaling Pathways between Cancer and Immune Cells)
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Review

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17 pages, 3623 KiB  
Review
Epithelial Mesenchymal Transition and Immune Response in Metaplastic Breast Carcinoma
by Silvia González-Martínez, Belén Pérez-Mies, David Pizarro, Tamara Caniego-Casas, Javier Cortés and José Palacios
Int. J. Mol. Sci. 2021, 22(14), 7398; https://doi.org/10.3390/ijms22147398 - 9 Jul 2021
Cited by 20 | Viewed by 3654
Abstract
Metaplastic breast carcinoma (MBC) is a heterogeneous group of infrequent triple negative (TN) invasive carcinomas with poor prognosis. MBCs have a different clinical behavior from other types of triple negative breast cancer (TNBC), being more resistant to standard chemotherapy. MBCs are an example [...] Read more.
Metaplastic breast carcinoma (MBC) is a heterogeneous group of infrequent triple negative (TN) invasive carcinomas with poor prognosis. MBCs have a different clinical behavior from other types of triple negative breast cancer (TNBC), being more resistant to standard chemotherapy. MBCs are an example of tumors with activation of epithelial–mesenchymal transition (EMT). The mechanisms involved in EMT could be responsible for the increase in the infiltrative and metastatic capacity of MBCs and resistance to treatments. In addition, a relationship between EMT and the immune response has been seen in these tumors. In this sense, MBC differ from other TN tumors showing a lower number of tumor-infiltrating lymphocytes (TILS) and a higher percentage of tumor cells expressing programmed death-ligand 1 (PD-L1). A better understanding of the relationship between the immune system and EMT could provide new therapeutic approaches in MBC. Full article
(This article belongs to the Special Issue Signaling Pathways between Cancer and Immune Cells)
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