Marine Antimicrobial Peptide Epinecidin-1 Inhibits Proliferation Induced by Lipoteichoic acid and Causes cell Death in non-small cell lung cancer Cells via Mitochondria Damage.

Epinecidin-1 Lipoteichoic acid Marine antimicrobial peptide Non-small-cell lung cancer Proliferation

Journal

Probiotics and antimicrobial proteins
ISSN: 1867-1314
Titre abrégé: Probiotics Antimicrob Proteins
Pays: United States
ID NLM: 101484100

Informations de publication

Date de publication:
31 Jul 2023
Historique:
accepted: 20 07 2023
medline: 31 7 2023
pubmed: 31 7 2023
entrez: 31 7 2023
Statut: aheadofprint

Résumé

Non-small cell lung cancer (NSCLC) is among the deadliest cancers worldwide. Despite the recent introduction of several new therapeutic approaches for the disease, improvements in overall survival and progression-free survival have been minimal. Conventional treatments for NSCLC include surgery, chemotherapy and radiotherapy. Except for surgery, these treatments can impair a patient's immune system, leaving them susceptible to bacterial infections. As such, Staphylococcus aureus infections are commonly seen in NSCLC patients receiving chemotherapy, and a major constituent of the S. aureus cell surface, lipoteichoic acid (LTA), is thought to stimulate NSCLC cancer cell proliferation. Thus, inhibition of LTA-mediated cell proliferation might be a useful strategy for treating NSCLC. Epinecidin-1 (EPI), a marine antimicrobial peptide, exhibits broad-spectrum antibacterial activity, and it also displays anti-cancer activity in glioblastoma and synovial sarcoma cells. Furthermore, EPI has been shown to inhibit LTA-induced inflammatory responses in murine macrophages. Nevertheless, the anti-cancer and anti-LTA activities of EPI and the underlying mechanisms of these effects have not been fully tested in the context of NSCLC. In the present study, we demonstrate that EPI suppresses LTA-enhanced proliferation of NSCLC cells by neutralizing LTA and blocking its effects on toll-like receptor 2 and interleukin-8. Moreover, we show that EPI induces necrotic cell death via mitochondrial damage, elevated reactive oxygen species levels, and disrupted redox balance. Collectively, our results reveal dual anti-cancer activities of EPI in NSCLC, as the peptide not only directly kills cancer cells but it also blocks LTA-mediated enhancement of cell proliferation.

Identifiants

pubmed: 37523113
doi: 10.1007/s12602-023-10130-1
pii: 10.1007/s12602-023-10130-1
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Taipei Medical University - Wan Fang Hospital
ID : 110TMU-WFH-20 and 112-wf-eva-21
Organisme : Ministry of Science and Technology, Taiwan
ID : 109-2320-B-038-010-MY2; 110-2320-B-038 -023

Informations de copyright

© 2023. The Author(s).

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Auteurs

Hsin-Hsien Yu (HH)

Division of General Surgery, Department of Surgery, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan.
Division of General Surgery, Department of Surgery, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.

Luo-Yun Wu (LY)

School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.

Pei-Ling Hsu (PL)

Department of Anatomy, School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, 80708, Taiwan.
Department of Medical Research, Kaohsiung Medical University Hospital, Kaohsiung, 80708, Taiwan.

Chu-Wan Lee (CW)

Department of Nursing, National Tainan Junior College of Nursing, 78, Section 2, Minzu Road, West Central District, Tainan, 70007, Taiwan.

Bor-Chyuan Su (BC)

Department of Anatomy and Cell Biology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan. subc8265@tmu.edu.tw.
Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei, Taiwan. subc8265@tmu.edu.tw.

Classifications MeSH