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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...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
PeerJ Inc.
2023
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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. |
format | Online Article Text |
id | pubmed-10625348 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | PeerJ Inc. |
record_format | MEDLINE/PubMed |
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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