重新定位抗精神病药物阿立哌唑,使胰腺癌化疗更加敏感。

IF 5.7 3区 医学 Q1 MEDICINE, RESEARCH & EXPERIMENTAL International journal of molecular medicine Pub Date : 2025-01-01 Epub Date: 2024-11-14 DOI:10.3892/ijmm.2024.5458
Ye Jin Cho, Beom Seok Han, Soyeon Ko, Min Seok Park, Yun Ji Lee, Sang Eun Kim, Pureunchowon Lee, Han Gyeol Go, Shinyoung Park, Hyunho Lee, Sohee Kim, Eun-Ran Park, Kyung Hee Jung, Soon-Sun Hong
{"title":"重新定位抗精神病药物阿立哌唑,使胰腺癌化疗更加敏感。","authors":"Ye Jin Cho, Beom Seok Han, Soyeon Ko, Min Seok Park, Yun Ji Lee, Sang Eun Kim, Pureunchowon Lee, Han Gyeol Go, Shinyoung Park, Hyunho Lee, Sohee Kim, Eun-Ran Park, Kyung Hee Jung, Soon-Sun Hong","doi":"10.3892/ijmm.2024.5458","DOIUrl":null,"url":null,"abstract":"<p><p>Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy with limited therapeutic options. Cisplatin is a primary chemotherapeutic agent utilized in combination with other drugs or radiotherapy for PDAC treatment. However, the severe side effects of cisplatin often necessitate discontinuation of therapy and drug resistance in tumor cells poses significant clinical challenges. Therefore, the development of effective therapeutic strategies is imperative. The present study investigated whether repositioning of the antipsychotic drug aripiprazole could sensitize the anticancer activity of cisplatin in pancreatic cancer at doses calculated by the combination index. The findings indicated that aripiprazole combined with cisplatin to suppress pancreatic cancer cell growth. Notably, the combination notably increased the expression of apoptosis markers, including cleaved caspase‑3, compared with cisplatin alone. Additionally, this combination effectively decreased XIAP and MCL‑1 expression via mitochondrial membrane potential change as revealed by JC‑1 assay, thereby inducing apoptosis. Furthermore, in fluid shear stress assay, the combination of aripiprazole and cisplatin notably inhibited cell adhesion and tumor spheroid formation. Mechanistically, phospho‑kinase array profiles showed that the enhanced anticancer efficacy of the combination treatment could be attributed to the inhibition of STAT3 signaling, which led to a significant reduction in tumor growth in a pancreatic cancer animal model. The results showed that the repositioning of aripiprazole inhibits cancer cell growth by blocking the STAT3 signaling pathway and effectively enhancing cisplatin‑induced apoptosis, thereby suggesting that the combination of aripiprazole and cisplatin may be a potent chemotherapeutic strategy for the treatment of pancreatic cancer.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 1","pages":""},"PeriodicalIF":5.7000,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11573310/pdf/","citationCount":"0","resultStr":"{\"title\":\"Repositioning of aripiprazole, an anti‑psychotic drug, to sensitize the chemotherapy of pancreatic cancer.\",\"authors\":\"Ye Jin Cho, Beom Seok Han, Soyeon Ko, Min Seok Park, Yun Ji Lee, Sang Eun Kim, Pureunchowon Lee, Han Gyeol Go, Shinyoung Park, Hyunho Lee, Sohee Kim, Eun-Ran Park, Kyung Hee Jung, Soon-Sun Hong\",\"doi\":\"10.3892/ijmm.2024.5458\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy with limited therapeutic options. Cisplatin is a primary chemotherapeutic agent utilized in combination with other drugs or radiotherapy for PDAC treatment. However, the severe side effects of cisplatin often necessitate discontinuation of therapy and drug resistance in tumor cells poses significant clinical challenges. Therefore, the development of effective therapeutic strategies is imperative. The present study investigated whether repositioning of the antipsychotic drug aripiprazole could sensitize the anticancer activity of cisplatin in pancreatic cancer at doses calculated by the combination index. The findings indicated that aripiprazole combined with cisplatin to suppress pancreatic cancer cell growth. Notably, the combination notably increased the expression of apoptosis markers, including cleaved caspase‑3, compared with cisplatin alone. Additionally, this combination effectively decreased XIAP and MCL‑1 expression via mitochondrial membrane potential change as revealed by JC‑1 assay, thereby inducing apoptosis. Furthermore, in fluid shear stress assay, the combination of aripiprazole and cisplatin notably inhibited cell adhesion and tumor spheroid formation. Mechanistically, phospho‑kinase array profiles showed that the enhanced anticancer efficacy of the combination treatment could be attributed to the inhibition of STAT3 signaling, which led to a significant reduction in tumor growth in a pancreatic cancer animal model. The results showed that the repositioning of aripiprazole inhibits cancer cell growth by blocking the STAT3 signaling pathway and effectively enhancing cisplatin‑induced apoptosis, thereby suggesting that the combination of aripiprazole and cisplatin may be a potent chemotherapeutic strategy for the treatment of pancreatic cancer.</p>\",\"PeriodicalId\":14086,\"journal\":{\"name\":\"International journal of molecular medicine\",\"volume\":\"55 1\",\"pages\":\"\"},\"PeriodicalIF\":5.7000,\"publicationDate\":\"2025-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11573310/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"International journal of molecular medicine\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.3892/ijmm.2024.5458\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/11/14 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q1\",\"JCRName\":\"MEDICINE, RESEARCH & EXPERIMENTAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"International journal of molecular medicine","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.3892/ijmm.2024.5458","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/11/14 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
引用次数: 0

摘要

胰腺导管腺癌(PDAC)是一种致命的恶性肿瘤,治疗方法有限。顺铂是治疗 PDAC 的主要化疗药物,可与其他药物或放疗联合使用。然而,顺铂的严重副作用往往使治疗不得不中断,肿瘤细胞的耐药性也给临床带来了巨大挑战。因此,开发有效的治疗策略势在必行。本研究探讨了抗精神病药物阿立哌唑的重新定位是否能提高顺铂在胰腺癌中的抗癌活性,其剂量按联合指数计算。研究结果表明,阿立哌唑与顺铂联用可抑制胰腺癌细胞的生长。值得注意的是,与单用顺铂相比,阿立哌唑与顺铂联用可显著增加凋亡标志物的表达,包括裂解的caspase-3。此外,JC-1 试验显示,该组合能通过线粒体膜电位变化有效降低 XIAP 和 MCL-1 的表达,从而诱导细胞凋亡。此外,在流体剪切应力试验中,阿立哌唑和顺铂的组合能显著抑制细胞粘附和肿瘤球体的形成。从机理上讲,磷酸激酶阵列分析表明,联合疗法的抗癌效果增强可能是由于抑制了 STAT3 信号传导,从而显著降低了胰腺癌动物模型的肿瘤生长。结果表明,阿立哌唑的重新定位可通过阻断STAT3信号通路抑制癌细胞生长,并有效增强顺铂诱导的细胞凋亡,从而表明阿立哌唑和顺铂的联合治疗可能是治疗胰腺癌的有效化疗策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
Repositioning of aripiprazole, an anti‑psychotic drug, to sensitize the chemotherapy of pancreatic cancer.

Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy with limited therapeutic options. Cisplatin is a primary chemotherapeutic agent utilized in combination with other drugs or radiotherapy for PDAC treatment. However, the severe side effects of cisplatin often necessitate discontinuation of therapy and drug resistance in tumor cells poses significant clinical challenges. Therefore, the development of effective therapeutic strategies is imperative. The present study investigated whether repositioning of the antipsychotic drug aripiprazole could sensitize the anticancer activity of cisplatin in pancreatic cancer at doses calculated by the combination index. The findings indicated that aripiprazole combined with cisplatin to suppress pancreatic cancer cell growth. Notably, the combination notably increased the expression of apoptosis markers, including cleaved caspase‑3, compared with cisplatin alone. Additionally, this combination effectively decreased XIAP and MCL‑1 expression via mitochondrial membrane potential change as revealed by JC‑1 assay, thereby inducing apoptosis. Furthermore, in fluid shear stress assay, the combination of aripiprazole and cisplatin notably inhibited cell adhesion and tumor spheroid formation. Mechanistically, phospho‑kinase array profiles showed that the enhanced anticancer efficacy of the combination treatment could be attributed to the inhibition of STAT3 signaling, which led to a significant reduction in tumor growth in a pancreatic cancer animal model. The results showed that the repositioning of aripiprazole inhibits cancer cell growth by blocking the STAT3 signaling pathway and effectively enhancing cisplatin‑induced apoptosis, thereby suggesting that the combination of aripiprazole and cisplatin may be a potent chemotherapeutic strategy for the treatment of pancreatic cancer.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
International journal of molecular medicine
International journal of molecular medicine 医学-医学:研究与实验
CiteScore
12.30
自引率
0.00%
发文量
124
审稿时长
3 months
期刊介绍: The main aim of Spandidos Publications is to facilitate scientific communication in a clear, concise and objective manner, while striving to provide prompt publication of original works of high quality. The journals largely concentrate on molecular and experimental medicine, oncology, clinical and experimental cancer treatment and biomedical research. All journals published by Spandidos Publications Ltd. maintain the highest standards of quality, and the members of their Editorial Boards are world-renowned scientists.
期刊最新文献
[Retracted] PLGA/poloxamer nanoparticles loaded with EPAS1 siRNA for the treatment of pancreatic cancer in vitro and in vivo. Adrenic acid: A promising biomarker and therapeutic target (Review). Role of DNA methylation transferase in urinary system diseases: From basic to clinical perspectives (Review). [Corrigendum] A regulation loop between Nrf1α and MRTF‑A controls migration and invasion in MDA‑MB‑231 breast cancer cells. Advances in predicting breast cancer driver mutations: Tools for precision oncology (Review).
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1