The Role of Cathelicidin LL-37 in Cancer Development.
Piktel. Ewelina E; Niemirowicz. Katarzyna K; Wnorowska. Urszula U; Wątek. Marzena M; Wollny. Tomasz T; Głuszek. Katarzyna K; Góźdź. Stanisław S; Levental. Ilya I; Bucki. Robert R
Key Findings
- LL-37 can promote tumor growth in ovarian, lung and breast cancers
- LL-37 can suppress tumor growth in colon and gastric cancers
- Its actions depend on which membrane receptors are present in each cancer type
Practical Outcomes
- For biohackers, this means boosting or inhibiting LL-37 isn’t a simple, universal strategy for health or longevity. Until we know which tissues are affected and how, it’s safer to avoid trying to manipulate LL-37 levels outside of a clinical setting.
Summary
LL-37 is a natural peptide that can either help or hurt cancer growth depending on the organ. It’s higher in some cancers like ovarian, lung and breast, but lower in others like colon and stomach. The peptide works by binding to different cell‑surface receptors, so its effect changes with the type of tissue.
Abstract
LL-37 is a C-terminal peptide proteolytically released from 18 kDa human cathelicidin protein (hCAP18). Chronic infections, inflammation, tissue injury and tissue regeneration are all linked with neoplastic growth, and involve LL-37 antibacterial and immunomodulatory functions. Such a link points to the possible involvement of LL-37 peptide in carcinogenesis. An increasing amount of evidence suggests that LL-37 can have two different and contradictory effects--promotion or inhibition of tumor growth. The mechanisms are tissue-specific, complex, and depend mostly on the ability of LL-37 to act as a ligand for different membrane receptors whose expression varies on different cancer cells. Overexpression of LL-37 was found to promote development and progression of ovarian, lung and breast cancers, and to suppress tumorigenesis in colon and gastric cancer. This review explores and summarizes the current views on how LL-37 contributes to immunity, pathophysiology and cell signaling involved in malignant tumor growth.
Study Information
pubmed
2015
2015-09-22T00:00:00.000Z
10.1007/s00005-015-0359-5
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