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Cells
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Signaling at Crossroads between Tumor Microenvironment and Cancer Cells in...
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Signaling at Crossroads between Tumor Microenvironment and Cancer Cells in Tumor Progression

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

Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 9661

Special Issue Editors

Dr. Antonella Zannetti

E-Mail Website
Guest Editor
Institute of Biostructures and Bioimaging, National Research Council (IBB-CNR), 80145 Naples, Italy
Interests: molecular oncology; signal transduction; tumor microenvironment; molecular imaging in cancer; theranostic agents
Special Issues, Collections and Topics in MDPI journals
Dr. Laura Cerchia

E-Mail Website
Guest Editor
Institute of Experimental Endocrinology and Oncology "G. Salvatore" (IEOS), National Research Council (CNR), Naples, Italy
Interests: cell-SELEX; cancer biomarker discovery; cancer cell biology and signalling; targeted therapy; chemotherapy resistance
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Tumor growth and progression are closely dependent on and controlled by the microenvironment where the tumor develops (TME). The architecture surrounding the tumor is not static but is subjected to a continuous remodeling in response to the dynamic interplay between tumor cells and stroma. Tumor stroma is largely a product of the host and contains connective tissue, blood vessels and several types of resident and infiltrating host cells. Stromal cells are recruited into TME by numerous factors produced by tumor cells and here, they are “educated”, through an efficient cross-talk, to support tumor progression switching from a neutral or antitumorigenic role toward a pro-tumorigenic role. In addition to stromal cells, metabolic mediators are also involved, such as hypoxia, an essential metabolic element of the TME that may help to shape cellular plasticity and tumor heterogeneity. Hypoxic stress is predominantly caused by an abnormal formation of the vasculature of the rapidly growing tumor mass and the net result is heterogeneously distributed areas of low oxygen pressure. In this context, cancer cell adaptation allows for their survival and may give rise to heterogeneity and the emergence of therapy-resistant phenotypes. This Special Issue invites original research articles and timely reviews on aspects related to the interaction between tumor cells and multiple components of TME in tumor development, growth, metastasis and treatment response, including drug resistance and relapse as well as reprogramming of energy metabolism and evading immune suppression. It also aims to attract contributions highlighting recent insights and future directions in the development of therapeutic strategies targeting the interaction between tumor cells and TME components.

Dr. Antonella Zannetti
Dr. Laura Cerchia
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

  • tumor progression
  • tumor microenvironment
  • stromal cells
  • hypoxia
  • signal pathways
  • epithelial–mesenchymal transition
  • stemness
  • targeted therapy
  • biomarkers

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Published Papers (3 papers)

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Research

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20 pages, 6802 KiB  
Article
Tissue Inhibitor of Metalloproteinases-1 Overexpression Mediates Chemoresistance in Triple-Negative Breast Cancer Cells
by Lisa Agnello, Annachiara d’Argenio, Alessandra Caliendo, Roberto Nilo, Antonella Zannetti, Monica Fedele, Simona Camorani and Laura Cerchia
Cells 2023, 12(13), 1809; https://doi.org/10.3390/cells12131809 - 7 Jul 2023
Cited by 3 | Viewed by 1891
Abstract
Triple-negative breast cancer (TNBC) is among the most aggressive breast cancer subtypes. Despite being initially responsive to chemotherapy, patients develop drug-resistant and metastatic tumors. Tissue inhibitor of metalloproteinases-1 (TIMP-1) is a secreted protein with a tumor suppressor function due to its anti-proteolytic activity. [...] Read more.
Triple-negative breast cancer (TNBC) is among the most aggressive breast cancer subtypes. Despite being initially responsive to chemotherapy, patients develop drug-resistant and metastatic tumors. Tissue inhibitor of metalloproteinases-1 (TIMP-1) is a secreted protein with a tumor suppressor function due to its anti-proteolytic activity. Nevertheless, evidence indicates that TIMP-1 binds to the CD63 receptor and activates noncanonical oncogenic signaling in several cancers, but its role in mediating TNBC chemoresistance is still largely unexplored. Here, we show that mesenchymal-like TNBC cells express TIMP-1, whose levels are further increased in cells generated to be resistant to cisplatin (Cis-Pt-R) and doxorubicin (Dox-R). Moreover, public dataset analyses indicate that high TIMP-1 levels are associated with a worse prognosis in TNBC subjected to chemotherapy. Knock-down of TIMP-1 in both Cis-Pt-R and Dox-R cells reverses their resistance by inhibiting AKT activation. Consistently, TNBC cells exposed to recombinant TIMP-1 or TIMP-1-enriched media from chemoresistant cells, acquire resistance to both cisplatin and doxorubicin. Importantly, released TIMP-1 reassociates with plasma membrane by binding to CD63 and, in the absence of CD63 expression, TIMP-1-mediated chemoresistance is blocked. Thus, our results identify TIMP-1 as a new biomarker of TNBC chemoresistance and lay the groundwork for evaluating whether blockade of TIMP-1 signal is a viable treatment strategy. Full article
(This article belongs to the Special Issue Signaling at Crossroads between Tumor Microenvironment and Cancer Cells in Tumor Progression)
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14 pages, 2869 KiB  
Article
Inhibition of Bone Marrow-Mesenchymal Stem Cell-Induced Carbonic Anhydrase IX Potentiates Chemotherapy Efficacy in Triple-Negative Breast Cancer Cells
by Annachiara Sarnella, Ylenia Ferrara, Sandra Albanese, Daniela Omodei, Laura Cerchia, Giuseppina De Simone, Claudiu T. Supuran and Antonella Zannetti
Cells 2023, 12(2), 298; https://doi.org/10.3390/cells12020298 - 12 Jan 2023
Cited by 9 | Viewed by 2152
Abstract
Conventional chemotherapy represents the main systemic treatment used for triple-negative breast cancer (TNBC) patients, although many of them develop drug resistance. The hypoxic TME is the crucial driver in the onset of insensitivity to chemotherapy. In this research, we elucidated the role played [...] Read more.
Conventional chemotherapy represents the main systemic treatment used for triple-negative breast cancer (TNBC) patients, although many of them develop drug resistance. The hypoxic TME is the crucial driver in the onset of insensitivity to chemotherapy. In this research, we elucidated the role played by bone marrow-derived mesenchymal stem cells (BM-MSCs) in reducing cisplatin effects in TNBC. BT-549 and MDA-MB-231 cells, grown under hypoxic conditions in the presence of conditioned medium obtained from BM-MSCs (CM-MSCs), showed a strong cisplatin insensitivity and increased expression levels of carbonic anhydrase IX (CA IX). Therefore, we inhibited CM-MSC-induced CA IX by SLC-0111 to potentiate chemotherapy efficacy in TNBC cells. Our results showed that CM-MSCs under hypoxic conditions caused an increase in the ability of TNBC cells to form vascular structures, migrate and invade Matrigel. Cell treatment with cisplatin plus SLC-0111 was able to block these mechanisms, as well as the signaling pathways underlying them, such as p-AKT, p-ERK, CD44, MMP-2, vimentin, β-catenin, and N-cadherin, more effectively than treatment with single agents. In addition, a significant enhancement of apoptosis assessed by annexin V, caspase-3 expression and activity was also shown. Taken together, our results demonstrated the possibility, through CA IX inhibition, of returning TNBC cells to a more chemosensitive state. Full article
(This article belongs to the Special Issue Signaling at Crossroads between Tumor Microenvironment and Cancer Cells in Tumor Progression)
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Review

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29 pages, 1756 KiB  
Review
The Clinical Significance and Role of CXCL1 Chemokine in Gastrointestinal Cancers
by Jan Korbecki, Mateusz Bosiacki, Katarzyna Barczak, Ryta Łagocka, Dariusz Chlubek and Irena Baranowska-Bosiacka
Cells 2023, 12(10), 1406; https://doi.org/10.3390/cells12101406 - 17 May 2023
Cited by 8 | Viewed by 4752
Abstract
One area of cancer research is the interaction between cancer cells and immune cells, in which chemokines play a vital role. Despite this, a comprehensive summary of the involvement of C-X-C motif ligand 1 (CXCL1) chemokine (also known as growth-regulated gene-α (GRO-α), melanoma [...] Read more.
One area of cancer research is the interaction between cancer cells and immune cells, in which chemokines play a vital role. Despite this, a comprehensive summary of the involvement of C-X-C motif ligand 1 (CXCL1) chemokine (also known as growth-regulated gene-α (GRO-α), melanoma growth-stimulatory activity (MGSA)) in cancer processes is lacking. To address this gap, this review provides a detailed analysis of CXCL1’s role in gastrointestinal cancers, including head and neck cancer, esophageal cancer, gastric cancer, liver cancer (hepatocellular carcinoma (HCC)), cholangiocarcinoma, pancreatic cancer (pancreatic ductal adenocarcinoma), and colorectal cancer (colon cancer and rectal cancer). This paper presents the impact of CXCL1 on various molecular cancer processes, such as cancer cell proliferation, migration, and invasion, lymph node metastasis, angiogenesis, recruitment to the tumor microenvironment, and its effect on immune system cells, such as tumor-associated neutrophils (TAN), regulatory T (Treg) cells, myeloid-derived suppressor cells (MDSCs), and macrophages. Furthermore, this review discusses the association of CXCL1 with clinical aspects of gastrointestinal cancers, including its correlation with tumor size, cancer grade, tumor–node–metastasis (TNM) stage, and patient prognosis. This paper concludes by exploring CXCL1’s potential as a therapeutic target in anticancer therapy. Full article
(This article belongs to the Special Issue Signaling at Crossroads between Tumor Microenvironment and Cancer Cells in Tumor Progression)
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