XYA-2: a marine-derived compound targeting apoptosis and multiple signaling pathways in pancreatic cancer

Background Pancreatic cancer is a highly aggressive and fatal disease with limited treatment options and poor prognosis for patients. This study aimed to investigate the impact of XYA-2 {N-(3,7-dimethyl-2,6-octadienyl)-2-aza-2-deoxychaetoviridin A}, a nitrogenated azaphilon previously reported from...

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Main Authors: Xiaoqing Guan, Yun Li, Xiaodan Guan, Linfei Fan, Jieer Ying
Format: Article
Language:English
Published: PeerJ Inc. 2024-01-01
Series:PeerJ
Subjects:
Online Access:https://peerj.com/articles/16805.pdf
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author Xiaoqing Guan
Yun Li
Xiaodan Guan
Linfei Fan
Jieer Ying
author_facet Xiaoqing Guan
Yun Li
Xiaodan Guan
Linfei Fan
Jieer Ying
author_sort Xiaoqing Guan
collection DOAJ
description Background Pancreatic cancer is a highly aggressive and fatal disease with limited treatment options and poor prognosis for patients. This study aimed to investigate the impact of XYA-2 {N-(3,7-dimethyl-2,6-octadienyl)-2-aza-2-deoxychaetoviridin A}, a nitrogenated azaphilon previously reported from a deep-sea-derived fungus on the progression of pancreatic cancer cells. Methods The inhibitory effects of XYA-2 on cell proliferation, clonogenic potential, cell cycle progression, apoptosis, migration, and invasion were assessed using various assays. The CCK-8 assay, clone formation assay, flow cytometry assay, wound healing assay, and transwell assay were employed to evaluate cell proliferation, clonogenic potential, cell cycle progression, apoptosis, migration, and invasion, respectively. Moreover, we employed RNA-seq and bioinformatics analyses to uncover the underlying mechanism by which XYA-2 influences pancreatic cancer cells. The revealed mechanism was subsequently validated through qRT-PCR. Results Our results demonstrated that XYA-2 dose-dependently inhibited the proliferation of pancreatic cancer cells and induced cell cycle arrest and apoptosis. Additionally, XYA-2 exerted a significant inhibitory effect on the invasion and migration of cancer cells. Moreover, XYA-2 was found to regulate the expression of genes involved in multiple cancer-related pathways based on our RNA-seq and bioinformatics analysis. Conclusion These findings highlight the potential of XYA-2 as a promising therapeutic option for the treatment of pancreatic cancer.
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spelling doaj.art-f6b21db3c15642c5a8c439eb2c02db692024-01-18T15:05:22ZengPeerJ Inc.PeerJ2167-83592024-01-0112e1680510.7717/peerj.16805XYA-2: a marine-derived compound targeting apoptosis and multiple signaling pathways in pancreatic cancerXiaoqing Guan0Yun Li1Xiaodan Guan2Linfei Fan3Jieer Ying4Zhejiang Cancer Hospital, Hangzhou Institute of Medicine (HIM), Chinese Academy of Sciences, Zhejiang, ChinaZhejiang Cancer Hospital, Hangzhou Institute of Medicine (HIM), Chinese Academy of Sciences, Zhejiang, ChinaZhejiang Cancer Hospital, Hangzhou Institute of Medicine (HIM), Chinese Academy of Sciences, Zhejiang, ChinaZhejiang Cancer Hospital, Hangzhou Institute of Medicine (HIM), Chinese Academy of Sciences, Zhejiang, ChinaZhejiang Cancer Hospital, Hangzhou Institute of Medicine (HIM), Chinese Academy of Sciences, Zhejiang, ChinaBackground Pancreatic cancer is a highly aggressive and fatal disease with limited treatment options and poor prognosis for patients. This study aimed to investigate the impact of XYA-2 {N-(3,7-dimethyl-2,6-octadienyl)-2-aza-2-deoxychaetoviridin A}, a nitrogenated azaphilon previously reported from a deep-sea-derived fungus on the progression of pancreatic cancer cells. Methods The inhibitory effects of XYA-2 on cell proliferation, clonogenic potential, cell cycle progression, apoptosis, migration, and invasion were assessed using various assays. The CCK-8 assay, clone formation assay, flow cytometry assay, wound healing assay, and transwell assay were employed to evaluate cell proliferation, clonogenic potential, cell cycle progression, apoptosis, migration, and invasion, respectively. Moreover, we employed RNA-seq and bioinformatics analyses to uncover the underlying mechanism by which XYA-2 influences pancreatic cancer cells. The revealed mechanism was subsequently validated through qRT-PCR. Results Our results demonstrated that XYA-2 dose-dependently inhibited the proliferation of pancreatic cancer cells and induced cell cycle arrest and apoptosis. Additionally, XYA-2 exerted a significant inhibitory effect on the invasion and migration of cancer cells. Moreover, XYA-2 was found to regulate the expression of genes involved in multiple cancer-related pathways based on our RNA-seq and bioinformatics analysis. Conclusion These findings highlight the potential of XYA-2 as a promising therapeutic option for the treatment of pancreatic cancer.https://peerj.com/articles/16805.pdfPancreatic cancerXYA-2ApoptosisCell proliferationPancreatic cancer treatment
spellingShingle Xiaoqing Guan
Yun Li
Xiaodan Guan
Linfei Fan
Jieer Ying
XYA-2: a marine-derived compound targeting apoptosis and multiple signaling pathways in pancreatic cancer
PeerJ
Pancreatic cancer
XYA-2
Apoptosis
Cell proliferation
Pancreatic cancer treatment
title XYA-2: a marine-derived compound targeting apoptosis and multiple signaling pathways in pancreatic cancer
title_full XYA-2: a marine-derived compound targeting apoptosis and multiple signaling pathways in pancreatic cancer
title_fullStr XYA-2: a marine-derived compound targeting apoptosis and multiple signaling pathways in pancreatic cancer
title_full_unstemmed XYA-2: a marine-derived compound targeting apoptosis and multiple signaling pathways in pancreatic cancer
title_short XYA-2: a marine-derived compound targeting apoptosis and multiple signaling pathways in pancreatic cancer
title_sort xya 2 a marine derived compound targeting apoptosis and multiple signaling pathways in pancreatic cancer
topic Pancreatic cancer
XYA-2
Apoptosis
Cell proliferation
Pancreatic cancer treatment
url https://peerj.com/articles/16805.pdf
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AT yunli xya2amarinederivedcompoundtargetingapoptosisandmultiplesignalingpathwaysinpancreaticcancer
AT xiaodanguan xya2amarinederivedcompoundtargetingapoptosisandmultiplesignalingpathwaysinpancreaticcancer
AT linfeifan xya2amarinederivedcompoundtargetingapoptosisandmultiplesignalingpathwaysinpancreaticcancer
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