Host defense peptide Hymenochirin-1B induces lung cancer cell apoptosis and cell cycle arrest through the mitochondrial pathway

  • Biochem Biophys Res Commun. 2019 Apr 30;512(2):269-275. doi: 10.1016/j.bbrc.2019.03.029.
Yihan Zhang  1 ,  Changning Sun  1 ,  Guokai Xiao  1 ,  Yuchao Gu  2
Affiliations
  • 1. Key Laboratory of Marine Drugs, Ministry of Education, School of Medicine and Pharmacy, Ocean University of China, 5 Yushan Road, Qingdao, 266003, China; Laboratory for Marine Drugs and Bioproducts of Qingdao National Laboratory for Marine Science and Technology, Qingdao, 266200, China; Key Laboratory of Glycoscience & Glycotechnology of Shandong Province, Qingdao, 266003, China.
  • 2. Key Laboratory of Marine Drugs, Ministry of Education, School of Medicine and Pharmacy, Ocean University of China, 5 Yushan Road, Qingdao, 266003, China; Laboratory for Marine Drugs and Bioproducts of Qingdao National Laboratory for Marine Science and Technology, Qingdao, 266200, China; Key Laboratory of Glycoscience & Glycotechnology of Shandong Province, Qingdao, 266003, China. Electronic address: [email protected].
PMID: 30885438 DOI: 10.1016/j.bbrc.2019.03.029
Abstract

The antineoplastic activity of host defense peptide Hymenochirin-1B, has been extensively studied. However, the mechanism still remains unknown. In this study, linear peptide, Hymenochirin-1B, was synthesized via solid-phase peptide synthesis and evaluated for its Anticancer efficacy. We found Hymenochirin-1B induced lung Cancer cell Apoptosis and cell cycle arrest at the G0/G1 phase. Moreover, Hymenochirin-1B could enter the cells and colocalized with mitochondria. Furthermore, decrease of mitochondrial membrane potential, increase of Reactive Oxygen Species and the expression of apoptosis-associated protein (Bax/Bcl-2 ratio and activated Caspase-3) were observed in NCI-H1299 and A549 cells after Hymenochirin-1B treatment, suggesting that Hymenochirin-1B induced Apoptosis via mitochondrial pathway. Our results provide new insights on the Anticancer mechanism of Hymenochirin-1B, which may contribute to its further development into an antineoplastic drug in the future.

Keywords
Apoptosis; Hymenochirin-1B; Mitochondrial pathway.
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