Antimicrobial peptide LL-37 promotes the viability and invasion of skin squamous cell carcinoma by upregulating YB-1.
Wang. Wei W; Zheng. Yan Y; Jia. Jinjing J; Li. Changji C; Duan. Qiqi Q; Li. Ruilian R; Wang. Xin X; Shao. Yongping Y; Chen. Caifeng C; Yan. Huling H
Key Findings
- LL-37 increases YB‑1 protein levels in skin squamous cell carcinoma (SCC) cells.
- Higher YB‑1 levels make SCC cells more viable and invasive.
- The effect of LL-37 on YB‑1 depends on activation of the NF‑κB signaling pathway.
Practical Outcomes
- For biohackers, this study suggests that taking LL-37 could potentially promote skin cancer growth, especially if you have pre‑existing lesions or risk factors. It’s a cautionary signal to avoid LL‑37 supplementation unless safety is clearly established, and to monitor skin health closely if you’re exposed to high levels of this peptide.
Summary
The antimicrobial peptide LL-37, which some people think about using for its immune‑boosting effects, was found to make skin squamous cell cancer cells grow and spread faster by turning on a protein called YB‑1 through the NF‑κB pathway.
Abstract
Antimicrobial peptide LL-37 serves a function in the host defense against microbial invasion, and also regulates cell proliferation, immune activity and angiogenesis. Previous studies have reported that LL-37 participates in the development of numerous tumour types, such as ovarian cancer, lung cancer, melanoma and breast cancer. However, the function of LL-37 in the development of skin squamous cell carcinoma (SCC) has not yet been fully elucidated. The aim of the current study was to investigate how LL-37 promotes the expression of Y-box binding protein 1 (YB-1) in SCC. Short interfering RNA (siRNA) was used to inhibit the expression of YB-1, and <i>in vitro</i> MTT and Transwell migration assays were used to evaluate the effect of reduced YB-1 on the viability and invasion of A431 cells. A431 cells were stimulated with LL-37, and quantitative polymerase chain reaction, immunofluorescence and western blot analyses were used to detect changes in YB-1 expression. Mitogen-activated protein kinase kinase, mitogen-activated protein kinase and nuclear factor (NF)-κB signaling pathway inhibitors were also used to evaluate the mechanism of LL-37-induced YB-1 protein expression. It was found that YB-1 expression was increased in SCC tissue compared with normal tissue. Inhibiting YB-1 expression using siRNA significantly reduced the viability and suppressed the invasion of tumour cells (P<0.05 for both). LL-37 treatment at 0.05 µg/ml for 24 or 48 h significantly promoted YB-1 protein expression (P<0.05), and this was dependent on the NF-κB signaling pathway. In conclusion, the current study demonstrated that by upregulating the expression of YB-1, LL-37 can promote the occurrence and development of SCC, and this process involves the NF-κB signaling pathway.
Study Information
pubmed
2017
2017-06-06T00:00:00.000Z
10.3892/etm.2017.4546
18
38