Understand the source comparison
Cancer: pro-tumor versus anti-tumor duality
Nowhere is LL-37’s double-edged nature more explicit than in oncology, where the peptide can either promote or inhibit tumor growth depending on tissue type, receptor context, and concentration. Overexpression of LL-37 has been associated with the development
No winner is assigned.
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- Nowhere is LL-37’s double-edged nature more explicit than in oncology, where the peptide can either promote or inhibit tumor growth depending on tissue type, receptor context, and concentration. Overexpression of LL-37 has been associated with the development and progression of ovarian, lung, and breast cancers — where it can stimulate proliferation, angiogenesis, and the recruitment of tumor-supporting stromal cells — while in colon and gastric cancer LL-37 appears to suppress tumorigenesis, in part by inducing apoptosis. Concentration matters starkly: nanogram-per-milliliter levels may drive proliferation in one cancer cell type, whereas much higher doses of the same peptide reduce cell numbers. This receptor- and dose-dependent flip is the clearest possible illustration that LL-37 has no fixed moral valence in biology; its consequence is written by context.[14]
- Bacterial infection
- Membrane disruption, LPS neutralization, immune recruitment
- Protective
- Wound healing
- Angiogenesis, re-epithelialization
- Rosacea
- Aberrant kallikrein-processed fragments drive inflammation/angiogenesis
- Pathogenic
- Psoriasis
- LL-37–self-DNA/RNA complexes activate pDCs (TLR9/TLR7-8); autoantigen
- Lupus (SLE)
- NET-associated LL-37–DNA complexes drive interferon/autoimmunity
- Atherosclerosis
- Plaque inflammation, smooth-muscle death, thrombosis
- Cancer
- Pro-tumor (ovary, lung, breast) or anti-tumor (colon, gastric)
- Context-dependent