Peer-influenced content. Sources you trust. No registration required. This is HCN.

MD NewslineThe Role of Interleukin-1ß in Breast Cancer Bone Metastasis

IL-1B’s multifaceted role in breast cancer bone metastasis emphasizes its potential as a therapeutic target, linking chronic inflammation to metastatic progression and the vicious cycle of bone resorption.

Interleukin-1B (IL-1B), a potent pro-inflammatory cytokine, plays a critical role in breast cancer progression and metastasis, particularly in bone. This comprehensive review examines IL-1B’s involvement in tumor growth, epithelial-to-mesenchymal transition (EMT), and the establishment of metastatic niches in bone. It also explores the cytokine’s influence on the vicious cycle of bone metastasis and evaluates preclinical studies on IL-1B inhibition as a therapeutic strategy. Combining anti-IL-1 therapies with standard treatments shows promise, though the complexity of IL-1B’s effects on primary and metastatic tumors necessitates further investigation.

Key Points:

  • IL-1B’s Role in Tumor Progression:
    • IL-1B promotes EMT, facilitating tumor cell migration and invasion.
    • It regulates inflammation within the tumor microenvironment, aiding tumor growth.
    • IL-1B enhances angiogenesis, supporting tumor expansion and dissemination.
  • Bone Metastatic Niche Formation:
    • IL-1B upregulates in the bone microenvironment upon the arrival of breast cancer cells.
    • It promotes the creation of a conducive niche for metastatic cells.
    • IL-1B stimulates the activity of osteoblasts and endothelial cells, expanding the metastatic niche.
  • Vicious Cycle of Bone Metastasis:
    • IL-1B is pivotal in the vicious cycle of bone metastasis, enhancing osteoclast activity and bone resorption.
    • It triggers the release of growth factors from the bone matrix, fueling further tumor growth.
    • IL-1B’s role in osteoclast differentiation leads to excessive bone destruction.
  • Therapeutic Implications:
    • Inhibition of IL-1B signaling reduces bone metastasis in preclinical models.
    • Anti-IL-1 therapies, such as Anakinra, show potential in combination with chemotherapy and immunotherapy.
    • Effective targeting of IL-1B may require consistent suppression to prevent dormant cell reactivation and metastatic outgrowth.
  • Molecular Mechanisms:
    • IL-1B activation involves cleavage by Caspase-1, initiating a cascade that activates NF-κB, STAT3, and other signaling pathways.
    • IL-1B synergizes with TGFβ, promoting pro-tumorigenic environments through IL-17 and IL-22 secretion.
    • It enhances breast cancer cell aggressiveness via upregulation of IL-6 and IL-8.
  • Preclinical Study Findings:
    • Genetic overexpression of IL-1B in breast cancer cells induces EMT and increases migratory and invasive capabilities.
    • IL-1B facilitates tumor cell extravasation and homing to the bone marrow.
    • Pharmacological inhibition of IL-1 signaling shows reduced metastatic outgrowth in mouse models.

Breast cancer (BC) is mainly diagnosed in early stages (90–95%), however 20–30% of these patients become metastatic and to this day incurable. Bone is the single most frequent site for metastases and is involved in about 70% of all metastatic patients. (Ecancermedicalscience)

More on Metastasis

The Healthcare Communications Network is owned and operated by IQVIA Inc.

Click below to leave this site and continue to IQVIA’s Privacy Choices form