Human cathelicidin antimicrobial peptide suppresses proliferation, migration and invasion of oral carcinoma HSC-3 cells via a novel mechanism involving caspase-3 mediated apoptosis.

Human cathelicidin antimicrobial peptide and its active product, LL‑37 (CAMP/LL‑37), exhibit a broad spectrum of antimicrobial effects. An increasing number of studies have shown that human CAMP/LL‑37 also serves significant roles in various types of cancer. The primary aims of the present study were to investigate the roles and mechanisms of human CAMP/LL‑37 in oral squamous cell carcinoma (OSCC) cells. The results indicated that either LL‑37 C‑terminal deletion mutants (CDEL) or CAMP stable expression in HSC‑3 cells reduced colony formation, proliferation, migration and invasion ability of the cells. Expression analysis demonstrated that either CDEL or CAMP stable expression in HSC‑3 cells induced caspase‑3 mediated apoptosis via the P53‑Bcl‑2/BAX signalling pathway, whereas the levels of cell cycle‑related proteins, cyclin B1 and PKR‑like ER kinase, were significantly upregulated in the CAMP, but not in the CDEL overexpressing cells. Transcriptional profile comparisons revealed that CDEL or CAMP stable expression in HSC‑3 cells upregulated expression of genes involved in the IL‑17‑dependent pathway compared with the control. Taken together, these results suggest that CAMP may act as a tumour suppressor in OSCC cells, and the underlying mechanism involves the induction of caspase‑3 mediated apoptosis via the P53‑Bcl‑2/BAX signalling pathway.