New Targets and Therapeutic Approaches Based on Molecular Mechanisms in Tumorigenesis and Cancer Metastasis

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

Deadline for manuscript submissions: closed (31 January 2025) | Viewed by 1897

Special Issue Editor


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Guest Editor
Health & Biomedicine unit of LEITAT Technological Center, Barcelona Science Park, 08028 Barcelona, Spain
Interests: cancer; metastasis; tumor microenvironment; antibody engineering; alarmin; angiogenesis; therapy; diagnosis; fibrosis; immuno-oncology

Special Issue Information

Dear Colleagues,

Tumorigenesis and cancer metastasis encompass various molecular interactions and cellular processes that contribute to the initiation, progression, and spread of cancer. The deep knowledge covering all these aspects allows the scientific and medical community to provide new diagnostic tools and therapeutic approaches to fight against this devastating disease.

This Special Issue will welcome relevant articles and reviews that address the most revealing and crucial events, including but not limited to the following:

  • The tumor microenvironment is a supportive ecosystem, creating a favorable niche for cancer cells to thrive. It involves various cell types (cancer, immune, endothelial, fibroblasts) as well as extracellular matrix components, growth factors, and cytokines. Crosstalk between all these components is key to promote tumor growth, invasion, and metastasis;
  • The dysregulation of cell signaling pathways is a hallmark of cancer. Understanding how cell signaling pathways contribute to tumorigenesis and metastasis provides cutting-edge insights into the regulation of cell proliferation, survival, migration, and invasion;
  • Genetic mutations, as well as epigenetic alterations, such as DNA methylation, histone modifications, and non-coding RNA deregulation, highly contribute to cancer development and progression;
  • Cancer stem cells are closely involved in tumor initiation, progression, metastasis, and resistance to therapy. The therapeutic targeting of cancer stem cells holds promise for improving cancer treatment outcomes;
  • Cutting-edge knowledge about cancer progression and metastatic dissemination has led to the identification of new therapeutic targets. Similarly, new therapeutic approaches, such as targeted therapies, antibodies and antibody-like molecules, immuno-oncology, advanced therapies (gene, cell, and tissue engineering), etc., have been developed to specifically inhibit key molecules or pathways involved in cancer progression.

Dr. Francesc Mitjans
Guest Editor

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Keywords

  • metastasis
  • cancer
  • therapy
  • precision medicine
  • cancer stem cells
  • immuno-oncology
  • tumor microenvironment
  • antibody

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Published Papers (2 papers)

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Research

15 pages, 4180 KiB  
Article
Enhanced Expression of TRIM46 in Ovarian Cancer Cells Induced by Tumor-Associated Macrophages Promotes Invasion via the Wnt/β-Catenin Pathway
by Yi-Yue Wang, Min-Jun Choi, Jin-Hyung Kim and Jung-Hye Choi
Cells 2025, 14(3), 214; https://doi.org/10.3390/cells14030214 - 2 Feb 2025
Viewed by 430
Abstract
Metastasis presents significant challenges in ovarian cancer treatment. Tumor-associated macrophages (TAMs) within the tumor microenvironment (TME) facilitate metastasis through epithelial-mesenchymal transition, yet the molecular underlying mechanisms are not fully understood. Here, we identified that tripartite motif-containing 46 (TRIM46) is significantly upregulated in ovarian [...] Read more.
Metastasis presents significant challenges in ovarian cancer treatment. Tumor-associated macrophages (TAMs) within the tumor microenvironment (TME) facilitate metastasis through epithelial-mesenchymal transition, yet the molecular underlying mechanisms are not fully understood. Here, we identified that tripartite motif-containing 46 (TRIM46) is significantly upregulated in ovarian cancer cells treated with a conditioned medium derived from macrophages stimulated by ovarian cancer cells (OC-MQs). Furthermore, TRIM46 was highly expressed in late-stage ovarian cancer patients and was associated with poor prognosis. Silencing of TRIM46 suppressed cancer cell invasion stimulated by OC-MQ and mesenchymal marker expression without affecting cell viability. Gene set enrichment analysis showed that the Wnt/β-catenin pathway is enriched in the high-TRIM46 expression group. Importantly, the inhibition of TRIM46-mediated β-catenin nuclear translocation and ovarian cancer cell invasion was reversed by CHIR99021, a Wnt/β-catenin activator. Additionally, C-X-C motif chemokine ligand 8 (CXCL8) was identified as being highly expressed in peritoneal MQs from the ascites of ovarian cancer patients and was positively correlated with C-X-C chemokine receptor 1/2 (CXCR1/2) expression in tumor cells. Notably, pre-treatment with reparixin, a CXCR1/2 inhibitor, blocked OC-MQ-induced TRIM46 expression and cell invasion. These results suggest that CXCL8 derived from TAMs promotes human ovarian cancer cell invasion via the Wnt/β-catenin pathway by upregulating TRIM46. Full article
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26 pages, 3140 KiB  
Article
SIRT2 Inhibition by AGK2 Promotes Perinuclear Cytoskeletal Organisation and Reduces Invasiveness of MDA-MB-231 Triple-Negative Breast Cancer Cells in Confined In Vitro Models
by Emily Jessop, Natalie Young, Beatriz Garcia-Del-Valle, Jack T. Crusher, Boguslaw Obara and Iakowos Karakesisoglou
Cells 2024, 13(23), 2023; https://doi.org/10.3390/cells13232023 - 7 Dec 2024
Viewed by 1119
Abstract
Triple-negative breast cancer (TNBC) is a highly aggressive breast cancer subtype characterised by the absence of targetable hormone receptors and increased metastatic rates. As nuclear softening strongly contributes to TNBC’s enhanced metastatic capacity, increasing the nuclear stiffness of TNBC cells may present a [...] Read more.
Triple-negative breast cancer (TNBC) is a highly aggressive breast cancer subtype characterised by the absence of targetable hormone receptors and increased metastatic rates. As nuclear softening strongly contributes to TNBC’s enhanced metastatic capacity, increasing the nuclear stiffness of TNBC cells may present a promising therapeutic avenue. Previous evidence has demonstrated the ability of Sirtuin 2 (SIRT2) inhibition to induce cytoskeletal reorganisation, a key factor in regulating nuclear mechanics. Thus, our study aimed to investigate the effect of SIRT2 inhibition on the nuclear mechanics and migratory behaviour of TNBC cells. To achieve this, SIRT2 was pharmacologically inhibited in MDA-MB-231 cells using AGK2, a SIRT2-specific inhibitor. Although SIRT2 inhibition had no effect on LINC complex composition, the AGK2-treated MDA-MB-231 cells displayed more prominent perinuclear organisations of acetylated α-tubulin, vimentin, and F-actin. Additionally, the nuclei of the AGK2-treated MDA-MB-231 cells exhibited greater resistance to collapse under osmotic shock. Scratch-wound assays also revealed that SIRT2 inhibition led to polarity defects in the MDA-MB-231 cells, while in vitro space-restrictive invasion assays highlighted their reduced migratory capacity upon AGK2 treatment. Taken together, our findings suggest that SIRT2 inhibition promotes a perinuclear cytoskeletal organisation in MDA-MB-231 cells, which enhances their nuclear rigidity and impedes their invasion through confined spaces in vitro. Full article
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