Harnessing the Tumor Microenvironment and Signaling Pathways for Precision Cancer Therapy

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

Deadline for manuscript submissions: 28 February 2025 | Viewed by 2852

Special Issue Editors


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Guest Editor
Department of Small Animal Clinical Sciences, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, SK S7N 5B4, Canada
Interests: cancer invasion and metastasis; receptor tyrosine kinases; animal models of cancer; comparative oncology; cancer biomarker discovery

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Guest Editor
Laboratory Medicine, Department of Pathology, College of Medicine, University of Saskatchewan, Saskatoon, SK S7N 5E5, Canada
Interests: cancer cell biology; tumor biology; signal transduction; receptors; xenografts; tumor-initiating cells

Special Issue Information

Dear Colleagues,

This Special Issue, entitled "Harnessing the Tumor Microenvironment and Signaling Pathways for Precision Cancer Therapy," aims to explore the intricate dynamics of the tumor microenvironment (TME) and the signaling pathways that drive cancer progression. By focusing on the TME, this Special Issue will delve into how various components, such as immune cells, stromal cells, and the extracellular matrix, interact with cancer cells to influence tumor behavior and response to treatments. Additionally, it will highlight the significance of signaling pathways in tumor development and metastasis, presenting novel insights into their potential as therapeutic targets. Our goal is to present cutting-edge research and innovative approaches that leverage the TME and signaling pathways to develop precision therapies tailored to individual patients. This Special Issue will include contributions from leading researchers and clinicians, covering topics such as the role of the TME in immune evasion, the impact of metabolic pathways on tumor growth, and the latest advancements in targeting key signaling molecules for improved therapeutic outcomes. Through a comprehensive examination of these areas, this Special Issue aims to pave the way for more effective and personalized cancer treatment strategies.

Dr. Behzad M. Toosi
Dr. Andrew Freywald
Guest Editors

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Keywords

  • tumor microenvironment (TME)
  • signaling pathways
  • precision cancer therapy
  • immune evasion
  • metabolic pathways
  • tumor–stroma interactions
  • therapeutic targets
  • personalized medicine
  • cancer metastasis
  • molecular oncology

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Published Papers (2 papers)

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Research

17 pages, 2210 KiB  
Article
TCF12 and LncRNA MALAT1 Cooperatively Harness High Cyclin D1 but Low β-Catenin Gene Expression to Exacerbate Colorectal Cancer Prognosis Independently of Metastasis
by Chia-Ming Wu, Chung-Hsing Chen, Kuo-Wang Tsai, Mei-Chen Tan, Fang-Yu Tsai, Shih-Sheng Jiang, Shang-Hung Chen, Wei-Shone Chen, Horng-Dar Wang and Tze-Sing Huang
Cells 2024, 13(24), 2035; https://doi.org/10.3390/cells13242035 - 10 Dec 2024
Viewed by 860
Abstract
Metastasis is a well-known factor worsening colorectal cancer (CRC) prognosis, but mortality mechanisms in non-metastatic patients with poor outcomes are less understood. TCF12 is a transcription factor that can be physically associated with the long non-coding RNA MALAT1, creating an alliance with correlated [...] Read more.
Metastasis is a well-known factor worsening colorectal cancer (CRC) prognosis, but mortality mechanisms in non-metastatic patients with poor outcomes are less understood. TCF12 is a transcription factor that can be physically associated with the long non-coding RNA MALAT1, creating an alliance with correlated expression levels in CRC patients. This TCF12–MALAT1 alliance is linked to poorer prognosis independently of age and metastasis. To identify the downstream effects responsible for this outcome, we analyzed 2312 common target genes of TCF12 and MALAT1, finding involvement in pathways like Aurora B, ATM, PLK1, and non-canonical WNT. We investigated the impact of WNT downstream genes CTNNB1 and CCND1, encoding β-catenin and cyclin D1, respectively, on survival in CRC patients with this alliance. Tumors with higher TCF12 and MALAT1 gene expressions alongside increased β-catenin gene expressions were classified as having a “Pan-CMS-2 pattern”, showing relatively better prognoses. Conversely, tumors with high TCF12, MALAT1, and cyclin D1 gene expressions but low β-catenin expression were categorized as “TMBC pattern”, associated with poor survival, with survival rates dropping sharply from 60% at one year to 30% at three years. This suggests that targeting cyclin D1-associated CDK4/6 could potentially reduce early mortality risks in TMBC patients, supporting personalized medicine approaches. Full article
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14 pages, 5248 KiB  
Article
α-Parvin Expression in Breast Cancer Tissues: Correlation with Clinical Parameters and Prognostic Significance
by Midori Takeda, Hiroaki Ito, Keisuke Kitahata, Sota Sato, Akira Nishide, Kanae Gamo, Shunsuke Managi, Tohru Tezuka, Akihiko Yoshizawa and Minsoo Kim
Cells 2024, 13(18), 1572; https://doi.org/10.3390/cells13181572 - 19 Sep 2024
Cited by 1 | Viewed by 1556
Abstract
Stromal cells play a critical role in the tumor microenvironment of breast cancer (BC), as they are recruited by tumor cells and regulate the metastatic spread. Though high expression of α-parvin, a member of the parvin family of actin-binding proteins, is reported to [...] Read more.
Stromal cells play a critical role in the tumor microenvironment of breast cancer (BC), as they are recruited by tumor cells and regulate the metastatic spread. Though high expression of α-parvin, a member of the parvin family of actin-binding proteins, is reported to be associated with a poor prognosis and metastasis in several cancers, its role in carcinogenesis has not been thoroughly explored. Therefore, we aimed to examine the expression of α-parvin in BC patients by compartmentalizing and quantifying tissues to determine whether α-parvin can be a potential therapeutic target. We performed immunohistochemical (IHC) staining of α-parvin in BC tissues, and the IHC scores were calculated in the overall tissue, stroma, and epithelium using image analysis software. The expression of α-parvin was significantly higher in BC tissues (p = 0.0002) and BC stroma (p < 0.0001) than in normal tissues. Furthermore, all α-parvin scores were significantly positively correlated with the proliferation marker Ki67. The overall and stroma scores are associated with the tumor, (lymph) node, and metastasis (TNM) classification, stage, and grade. These results suggest that high expression of α-parvin in stroma is associated with BCs and might be a new predictive marker for diagnosing BC. Full article
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