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Published on: July 5, 2022
Neural regulation of cancer: from mechanobiology to inflammation
Tae-Hyung Kim1, Amy C Rowat2, Erica K Sloan3
1Cousins Center for PNI, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, Los Angeles, CA, USA; Department of Integrative Biology and Physiology, University of California, Los Angeles, Los Angeles, CA, USA.
Abstract:
Despite recent progress in cancer research, the exact nature of malignant transformation and its progression is still not fully understood. Particularly metastasis, which accounts for most cancer death, is a very complex process, and new treatment strategies require a more comprehensive understanding of underlying regulatory mechanisms. Recently, the sympathetic nervous system (SNS) has been implicated in cancer progression and beta-blockers have been identified as a novel strategy to limit metastasis. This review discusses evidence that SNS signaling regulates metastasis by modulating the physical characteristics of tumor cells, tumor-associated immune cells and the extracellular matrix (ECM). Altered mechanotype is an emerging hallmark of cancer cells that is linked to invasive phenotype and treatment resistance. Mechanotype also influences crosstalk between tumor cells and their environment, and may thus have a critical role in cancer progression. First, we discuss how neural signaling regulates metastasis and how SNS signaling regulates both biochemical and mechanical properties of tumor cells, immune cells and the ECM. We then review our current knowledge of the mechanobiology of cancer with a focus on metastasis. Next, we discuss links between SNS activity and tumor-associated inflammation, the mechanical properties of immune cells, and how the physical properties of the ECM regulate cancer and metastasis. Finally, we discuss the potential for clinical translation of our knowledge of cancer mechanobiology to improve diagnosis and treatment.
Insights
The sympathetic nervous system (SNS) influences cancer metastasis by altering cell and matrix mechanics. Understanding these mechanobiology principles may lead to new treatments targeting cancer progression and spread.
Area of Science:
- Oncology
- Mechanobiology
- Neuroscience
Background:
- Cancer metastasis remains a leading cause of death, necessitating deeper understanding of its regulatory mechanisms.
- The sympathetic nervous system (SNS) is increasingly recognized for its role in cancer progression, with beta-blockers showing potential in limiting metastasis.
- Altered cell and matrix physical characteristics (mechanotype) are emerging hallmarks of cancer, linked to invasiveness and treatment resistance.
Purpose of the Study:
- To review the evidence linking SNS signaling to cancer metastasis through modulation of physical characteristics.
- To explore the role of cancer mechanobiology, particularly in metastasis.
- To discuss the clinical translation potential of mechanobiology insights for cancer diagnosis and treatment.
Main Methods:
- Review of existing literature on SNS signaling, cancer progression, and mechanobiology.
- Analysis of how neural signaling impacts tumor cell, immune cell, and extracellular matrix (ECM) properties.
- Examination of the interplay between SNS activity, inflammation, immune cell mechanics, and ECM properties.
Main Results:
- SNS signaling influences metastasis by altering the physical and biochemical properties of tumor cells, immune cells, and the ECM.
- Cancer cell mechanotype is critical for invasive phenotypes, treatment resistance, and cell-environment crosstalk.
- SNS activity is linked to tumor-associated inflammation and influences the mechanical properties of immune cells and the ECM.
Conclusions:
- Understanding the mechanobiology of cancer, particularly how SNS signaling affects physical characteristics, is crucial for developing novel anti-metastasis strategies.
- Targeting mechanobiological processes influenced by the SNS offers potential for improved cancer diagnosis and treatment.
- Further research into the physical aspects of cancer progression driven by neural signaling is warranted for clinical applications.
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