C-terminal domain of human CAP18 antimicrobial peptide induces apoptosis in oral squamous cell carcinoma SAS-H1 cells.
Okumura. Kazuhiko K; Itoh. Akifumi A; Isogai. Emiko E; Hirose. Kimiharu K; Hosokawa. Yoichiro Y; Abiko. Yoshihiro Y; Shibata. Takatoshi T; Hirata. Michimasa M; Isogai. Hiroshi H
Key Findings
- The 27‑amino‑acid fragment hCAP18(109-135) induces apoptosis in oral squamous cell carcinoma (SAS‑H1) cells.
- Apoptosis occurs without activation of caspases, suggesting a caspase‑independent pathway.
- The peptide causes mitochondrial depolarization in cancer cells but does not affect healthy gingival fibroblasts or keratinocytes.
Practical Outcomes
- At this stage the result is only an early‑stage lab observation; there is no dosage, delivery method, or safety data for humans. Biohackers cannot translate this into a real‑world protocol yet, and more animal and clinical research is needed before any anti‑cancer use could be considered.
Summary
A short piece of the human antimicrobial peptide LL-37 (called hCAP18(109-135)) can kill oral cancer cells in a dish by triggering a type of cell death that doesn't involve the usual caspase enzymes, while leaving normal gum cells unharmed. This effect is linked to messing up the cancer cells' mitochondria.
Abstract
Mammalian myeloid and epithelial cells express many antimicrobiotic peptides that contribute to innate host defense against invading microbes. In the present study, a 27-mer peptide of the C-terminal domain (hCAP18(109-135)) and analogs of the antimicrobial peptide human cathelicidin LL-37/human cationic antimicrobial protein 18 (hCAP18) were examined for tumoricidal activity. In vitro results showed that hCAP18(109-135) induced apoptosis in human oral squamous cell carcinoma (OSCC), SAS-H1 cells. The hCAP18(109-135) induced mitochondrial depolarization and apoptosis in SAS-H1 cells, but not in healthy human gingival fibroblasts (HGF) and human keratinocyte line HaCaT cells. Caspases were not activated during hCAP18(109-135)-induced apoptosis in SAS-H1 cells. The results indicate that hCAP18(109-135) may induce caspase-independent apoptosis in OSCC but not in normal cells. hCAP18(109-135) can therefore be a useful anti-tumor therapeutic agent in the treatment of OSCC.
Study Information
pubmed
2004
2004-08-30T00:00:00.000Z
10.1016/j.canlet.2004.04.006