Summary
This application note shows how tunable LunaX™ ECM was used to engineer humanised prostate tumour, bone, bone marrow and adipose niches. Across three peer-reviewed studies, these models captured species-specific bone metastasis, clinically relevant drug responses, stiffness-dependent cell behaviour and adipocyte-driven tumour growth.
What you’ll learn
- How to engineer humanised prostate tumour, bone, bone marrow and adipose microenvironments with tunable photocrosslinkable ECMs.
- How humanising the primary prostate tumour microenvironment changes cancer-cell homing to engineered human bone.
- How humanised bone constructs can reveal clinically relevant responses to bone-targeted therapies such as zoledronic acid.
- How ECM stiffness regulates osteoblast mineralisation and prostate cancer spheroid size across bone marrow-like and cortical bone-like conditions.
- How incorporating human adipocytes creates a more complete fatty bone niche for studying prostate cancer growth and metabolic crosstalk.
Key findings
- Humanising the orthotopic prostate tumour microenvironment reduced PC3-luc metastasis to humanised bone from 82% to 22% under the tested conditions (p = 0.02).
- Zoledronic acid reduced metastatic burden in humanised bone constructs from a mean total flux of 6.38 × 10⁴ to 1.27 × 10⁴ p·s⁻¹ (p < 0.01) and decreased osteoclast activity.
- Prostate cancer cells preferentially colonised humanised bone, demonstrating species-specific metastatic tropism that murine bone alone did not reproduce.
- Lower-stiffness LunaX ECM increased osteoblast mineral deposition and produced larger LNCaP and C4-2B spheroids than higher-stiffness ECM (p < 0.001).
- Adding human adipocytes to the engineered bone niche increased C4-2B tumour growth in vivo, revealing a direct role for adipocyte–tumour crosstalk.
