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LL-37

Cathelicidin, hCAP-18, FALL-39, CAP-18

Quick Stats
Studies 2230
Trials 95
Score 2
2016 pubmed 18 citations

Antimicrobial peptide LL-37 promotes the proliferation and invasion of skin squamous cell carcinoma by upregulating DNA-binding protein A.

Wang. Wei W; Jia. Jinjing J; Li. Changji C; Duan. Qiqi Q; Yang. Jiao J; Wang. Xin X; Li. Ruilian R; Chen. Caifeng C; Yan. Huling H; Zheng. Yan Y

Key Findings

  • LL-37 increases proliferation, migration, and invasion of skin SCC (A341) cells.
  • LL-37 upregulates DNA‑binding protein A (dbpA) at both mRNA and protein levels.
  • Silencing dbpA or inhibiting NF‑κB (with PDTC) reverses the LL-37‑driven cancer cell effects.

Practical Outcomes

  • If you’re considering LL-37 for its antimicrobial or skin‑healing claims, be aware it may promote skin cancer cell growth, especially in existing lesions. Avoid topical or systemic LL-37 use if you have a history of skin SCC or precancerous spots, and monitor skin health closely when experimenting with immune‑modulating peptides.

Summary

The study shows that the antimicrobial peptide LL-37 can actually help skin squamous cell cancer cells grow and spread by turning on a protein called dbpA through the NF‑κB pathway, and blocking this pathway or the protein reduces the cancer‑like behavior.

Abstract

The antimicrobial peptide LL-37 not only contributes to the host defence against microbial invasion but also regulates immune activity, angiogenesis and cell proliferation. Studies have shown that LL-37 participates in the development of a variety of tumours, such as lung cancer, ovarian cancer, breast cancer and melanoma. However, the role of LL-37 in the development of skin squamous cell carcinoma (SCC) is not clear. The present study used immunohistochemistry to confirm that the expression of human DNA-binding protein A (dbpA) was increased in SCC tissues. After stimulating SCC A341 cells, LL-37 was shown promote the proliferation, migration and invasion of these malignant cells. LL-37 also promoted the upregulation of dbpA mRNA and protein expression. In addition, after using small interfering RNA to silence the normal dbpA expression in these malignant cells, the proliferation and invasion of the tumor cells were significantly reduced. When the NF-κB inhibitor PDTC was used to inhibit the process of LL-37-stimulated cells, it was found that the original upregulated expression of dbpA was downregulated. Overall, the present demonstrated that by upregulating the expression of dbpA, LL-37 can promote the proliferation and invasion of tumour cells, and that this process depends on the NF-κB signalling pathway.

Study Information

Provider

pubmed

Year

2016

Date

2016-07-15T00:00:00.000Z

DOI

10.3892/ol.2016.4865

Citations

18

References

37