Host-defence caerin 1.1 and 1.9 peptides suppress glioblastoma U87 and U118 cell proliferation through the modulation of mitochondrial respiration and induce the downregulation of CHI3L1

Yichen Wang; Furong Zhong; Fengyun Xiao; Junjie Li; Xiaosong Liu; Guoying Ni; Tianfang Wang; Wei Zhang

doi:10.1371/journal.pone.0304149

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Host-defence caerin 1.1 and 1.9 peptides suppress glioblastoma U87 and U118 cell proliferation through the modulation of mitochondrial respiration and induce the downregulation of CHI3L1

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Host-defence caerin 1.1 and 1.9 peptides suppress glioblastoma U87 and U118 cell proliferation through the modulation of mitochondrial respiration and induce the downregulation of CHI3L1

Yichen Wang, Furong Zhong, Fengyun Xiao, Junjie Li, Xiaosong Liu, Guoying Ni, Tianfang Wang and Wei Zhang

PLoS One, Vol.19(6), pp.1-25

2024

DOI: https://doi.org/10.1371/journal.pone.0304149

PMID: 38848430

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Abstract

Glioblastoma, the most aggressive form of brain cancer, poses a significant global health challenge with a considerable mortality rate. With the predicted increase in glioblastoma incidence, there is an urgent need for more effective treatment strategies. In this study, we explore the potential of caerin 1.1 and 1.9, host defence peptides derived from an Australian tree frog, in inhibiting glioblastoma U87 and U118 cell growth. Our findings demonstrate the inhibitory impact of caerin 1.1 and 1.9 on cell growth through CCK8 assays. Additionally, these peptides effectively curtail the migration of glioblastoma cells in a cell scratch assay, exhibiting varying inhibitory effects among different cell lines. Notably, the peptides hinder the G0/S phase replication in both U87 and U118 cells, pointing to their impact on the cell cycle. Furthermore, caerin 1.1 and 1.9 show the ability to enter the cytoplasm of glioblastoma cells, influencing the morphology of mitochondria. Proteomics experiments reveal intriguing insights, with a decrease in CHI3L1 expression and an increase in PZP and JUNB expression after peptide treatment. These proteins play roles in cell energy metabolism and inflammatory response, suggesting a multifaceted impact on glioblastoma cells. In conclusion, our study underscores the substantial anticancer potential of caerin 1.1 and 1.9 against glioblastoma cells. These findings propose the peptides as promising candidates for further exploration in the realm of glioblastoma management, offering new avenues for developing effective treatment strategies.

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Title: Host-defence caerin 1.1 and 1.9 peptides suppress glioblastoma U87 and U118 cell proliferation through the modulation of mitochondrial respiration and induce the downregulation of CHI3L1
Authors: Yichen Wang - Guangdong Pharmaceutical University
Furong Zhong - Guangdong Pharmaceutical University
Fengyun Xiao - Guangdong Pharmaceutical University
Junjie Li - Guangdong Pharmaceutical University
Xiaosong Liu - First People's Hospital of Foshan
Guoying Ni - Guangdong Pharmaceutical University
Tianfang Wang (Corresponding Author) - University of the Sunshine Coast, Queensland, Centre for Bioinnovation
Wei Zhang (Corresponding Author) - First People's Hospital of Foshan
Publication details: PLoS One, Vol.19(6), pp.1-25
Publisher: Public Library of Science
Date published: 2024
DOI: 10.1371/journal.pone.0304149
ISSN: 1932-6203
PMID: 38848430
Copyright note: © 2024 Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Data Availability: The mass spectrometry proteomics data have been deposited to the ProteomeXchange Consortium via the PRIDE partner repository with the dataset identifier PXD044941. The flow cytometric data of apoptosis experiment have been deposited to Flowrepository with the dataset link http://flowrepository.org/id/FR-FCM-Z764, while for the cell cycle experiment, the link to the data is http://flowrepository.org/id/FR-FCM-Z765.
Grant note: This study was supported in part by the First Affiliated Hospital of Guangdong Pharmaceutical University, Deng Feng project of Foshan First People’s Hospital (2019A008), Foshan municipal Government (2015AG1003), Guangdong Science and Technology Department (2016A020213001), National Science Foundation of Guangdong province (2020A1515010855), National Natural Science Foundation of China (31971355).
Organisation Unit: School of Science and Engineering - Legacy; GeneCology Research Centre - Legacy; School of Science, Technology and Engineering; Centre for Bioinnovation
Language: English
Record Identifier: 991043497802621
Output Type: Journal article

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