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A benzochalcone derivative synchronously induces apoptosis and ferroptosis in pancreatic cancer cells

BACKGROUND: Pancreatic cancer is a highly aggressive and lethal disease with limited treatment options. In this study, we investigated the potential therapeutic effects of compound KL-6 on pancreatic cancer cells. METHODS: The study involved assessing the inhibitory effects of KL-6 on cell prolifera...

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Autores principales: Guan, Xiaoqing, Zhao, Bing, Guan, Xiaodan, Dong, Jinyun, Ying, Jieer
Formato: Online Artículo Texto
Lenguaje:English
Publicado: PeerJ Inc. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10625348/
https://www.ncbi.nlm.nih.gov/pubmed/37927794
http://dx.doi.org/10.7717/peerj.16291
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author Guan, Xiaoqing
Zhao, Bing
Guan, Xiaodan
Dong, Jinyun
Ying, Jieer
author_facet Guan, Xiaoqing
Zhao, Bing
Guan, Xiaodan
Dong, Jinyun
Ying, Jieer
author_sort Guan, Xiaoqing
collection PubMed
description BACKGROUND: Pancreatic cancer is a highly aggressive and lethal disease with limited treatment options. In this study, we investigated the potential therapeutic effects of compound KL-6 on pancreatic cancer cells. METHODS: The study involved assessing the inhibitory effects of KL-6 on cell proliferation, clonogenic potential, cell cycle progression, apoptosis, migration, and invasion. Additionally, we examined the action mechanism of KL-6 by RNA-seq and bioinformatic analysis and validated by qRT-PCR and western blot in pancreatic cancer cells. RESULTS: Our results demonstrated that KL-6 effectively inhibited the growth of pancreatic cancer cells in a dose-dependent manner. It induced G2/M phase cell cycle arrest and apoptosis, disrupting the cell cycle progression and promoting cell death. KL-6 also exhibited inhibitory effects on cell migration and invasion, suggesting its potential to suppress the metastatic properties of pancreatic cancer cells. Furthermore, KL-6 modulated the expression of genes involved in various cancer-related pathways including apoptosis and ferroptosis. CONCLUSION: These findings collectively support the potential of KL-6 as a promising therapeutic option for pancreatic cancer treatment. Further research is needed to fully understand the underlying mechanisms and evaluate the clinical efficacy of KL-6 in pancreatic cancer patients.
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spelling pubmed-106253482023-11-05 A benzochalcone derivative synchronously induces apoptosis and ferroptosis in pancreatic cancer cells Guan, Xiaoqing Zhao, Bing Guan, Xiaodan Dong, Jinyun Ying, Jieer PeerJ Biochemistry BACKGROUND: Pancreatic cancer is a highly aggressive and lethal disease with limited treatment options. In this study, we investigated the potential therapeutic effects of compound KL-6 on pancreatic cancer cells. METHODS: The study involved assessing the inhibitory effects of KL-6 on cell proliferation, clonogenic potential, cell cycle progression, apoptosis, migration, and invasion. Additionally, we examined the action mechanism of KL-6 by RNA-seq and bioinformatic analysis and validated by qRT-PCR and western blot in pancreatic cancer cells. RESULTS: Our results demonstrated that KL-6 effectively inhibited the growth of pancreatic cancer cells in a dose-dependent manner. It induced G2/M phase cell cycle arrest and apoptosis, disrupting the cell cycle progression and promoting cell death. KL-6 also exhibited inhibitory effects on cell migration and invasion, suggesting its potential to suppress the metastatic properties of pancreatic cancer cells. Furthermore, KL-6 modulated the expression of genes involved in various cancer-related pathways including apoptosis and ferroptosis. CONCLUSION: These findings collectively support the potential of KL-6 as a promising therapeutic option for pancreatic cancer treatment. Further research is needed to fully understand the underlying mechanisms and evaluate the clinical efficacy of KL-6 in pancreatic cancer patients. PeerJ Inc. 2023-11-01 /pmc/articles/PMC10625348/ /pubmed/37927794 http://dx.doi.org/10.7717/peerj.16291 Text en ©2023 Guan et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, reproduction and adaptation in any medium and for any purpose provided that it is properly attributed. For attribution, the original author(s), title, publication source (PeerJ) and either DOI or URL of the article must be cited.
spellingShingle Biochemistry
Guan, Xiaoqing
Zhao, Bing
Guan, Xiaodan
Dong, Jinyun
Ying, Jieer
A benzochalcone derivative synchronously induces apoptosis and ferroptosis in pancreatic cancer cells
title A benzochalcone derivative synchronously induces apoptosis and ferroptosis in pancreatic cancer cells
title_full A benzochalcone derivative synchronously induces apoptosis and ferroptosis in pancreatic cancer cells
title_fullStr A benzochalcone derivative synchronously induces apoptosis and ferroptosis in pancreatic cancer cells
title_full_unstemmed A benzochalcone derivative synchronously induces apoptosis and ferroptosis in pancreatic cancer cells
title_short A benzochalcone derivative synchronously induces apoptosis and ferroptosis in pancreatic cancer cells
title_sort benzochalcone derivative synchronously induces apoptosis and ferroptosis in pancreatic cancer cells
topic Biochemistry
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10625348/
https://www.ncbi.nlm.nih.gov/pubmed/37927794
http://dx.doi.org/10.7717/peerj.16291
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