Regulation of Breast Cancer Metastasis

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Medical Research".

Deadline for manuscript submissions: closed (31 October 2023)

Special Issue Editor


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Guest Editor
Department of Physiology, University of Pretoria, Pretoria 0007, South Africa
Interests: cellular regulation of cancer cell migration and adhesion; the role of GPCRs in cancer biology and metastasis; development of breast cancer organoid models; breast cancer diagnostics

Special Issue Information

Breast cancer is a complex disease, and comprehending the mechanisms driving its progression and metastasis is vital for developing effective therapies. Metastasis is a multifaceted process involving the intricate interplay of molecular signaling pathways and the tumor microenvironment, which culminates in cancer cell dissemination to distant organs.

 

Integrins are a family of transmembrane receptors that execute a crucial role in promoting cancer cell migration, invasion, and colonization in distant organs. For instance, integrin αvβ3 has been identified as a key molecule in breast cancer cell invasion and metastasis, owing to its ability to promote cell adhesion, migration, and survival.

 

Recent advances in genomics and transcriptomics have led to the identification of specific gene expression signatures linked with metastatic progression. These gene expression signatures include genes involved in cell migration and invasion, extracellular matrix remodeling, and immune evasion. Additionally, genetic mutations and alterations contribute to metastasis, including the activation of oncogenes and the inactivation of tumor suppressor genes.

 

Recent studies have highlighted the critical role of mechanotransduction and substrate stiffness in the regulation of breast cancer metastasis. Mechanotransduction involves the sensing and response of cells to mechanical signals in their environment. This process is regulated by various molecular mechanisms such as integrin-mediated adhesion, cytoskeletal remodeling, and signaling pathways including focal adhesion kinase (FAK), Rho GTPases, and the mitogen-activated protein (MAP) kinase pathway. On the other hand, substrate stiffness refers to the physical properties of the extracellular matrix, which can affect cell behavior, including cell adhesion, migration, and proliferation. Extracellular matrix stiffness promotes cancer cell invasion and metastasis by activating the mechanotransduction pathways that regulate cell migration and proliferation.

 

In summary, breast cancer metastasis is a multifaceted process involving the molecular signaling pathways, tumor microenvironment, and physical properties of the extracellular matrix. Integrins play a crucial role in promoting cancer cell movement through the extracellular matrix. In contrast, mechanotransduction and substrate stiffness are essential regulators of breast cancer metastasis, modulating cellular responses to mechanical stimuli and impacting cell behavior. A better understanding of these complex mechanisms is crucial for developing effective therapeutic strategies to prevent and treat breast cancer metastasis.

Dr. Iman Van Den Bout
Guest Editor

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Keywords

  • breast cancer
  • metastasis
  • mechanotransduction
  • integrins
  • actin
  • cytoskeleton
  • invasion
  • adhesion
  • EMT
  • genomics
  • proteomics
  • focal adhesion
  • motility

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