综合分析揭示帕酸吡啶在默克尔细胞癌中的治疗潜力。

Jiawen Yang, James T Lim, Paul Victor, Marcelo G Corona, Chen Chen, Hunain Khawaja, Qiong Pan, Gillian D Paine-Murrieta, Rick G Schnellmann, Denise J Roe, Prafulla C Gokhale, James A DeCaprio, Megha Padi
{"title":"综合分析揭示帕酸吡啶在默克尔细胞癌中的治疗潜力。","authors":"Jiawen Yang, James T Lim, Paul Victor, Marcelo G Corona, Chen Chen, Hunain Khawaja, Qiong Pan, Gillian D Paine-Murrieta, Rick G Schnellmann, Denise J Roe, Prafulla C Gokhale, James A DeCaprio, Megha Padi","doi":"10.1101/2023.11.01.565218","DOIUrl":null,"url":null,"abstract":"<p><p>Merkel Cell Carcinoma (MCC) is an aggressive neuroendocrine cutaneous malignancy arising from either ultraviolet-induced mutagenesis or Merkel cell polyomavirus (MCPyV) integration. Despite extensive research, our understanding of the molecular mechanisms driving the transition from normal cells to MCC remains limited. To address this knowledge gap, we assessed the impact of inducible MCPyV T antigens on normal human fibroblasts by performing RNA sequencing. Our data uncovered changes in expression and regulation of Wnt signaling pathway members. Building on this observation, we bioinformatically evaluated various Wnt pathway perturbagens for their ability to reverse the MCC gene expression signature and identified pyrvinium pamoate, an FDA-approved anthelminthic drug known for its anti-tumor activity in other cancers. Leveraging transcriptomic, network, and molecular analyses, we found that pyrvinium targets multiple MCC vulnerabilities. Pyrvinium not only reverses the neuroendocrine features of MCC by modulating canonical and non-canonical Wnt signaling but also inhibits cancer cell growth by activating p53-mediated apoptosis, disrupting mitochondrial function, and inducing endoplasmic reticulum stress. Finally, we demonstrated that pyrvinium reduces tumor growth in an MCC mouse xenograft model. These findings offer a new understanding of the role of Wnt signaling in MCC and highlight the utility of pyrvinium as a potential treatment for MCC.</p>","PeriodicalId":72407,"journal":{"name":"bioRxiv : the preprint server for biology","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10635082/pdf/","citationCount":"0","resultStr":"{\"title\":\"Integrative analysis reveals therapeutic potential of pyrvinium pamoate in Merkel cell carcinoma.\",\"authors\":\"Jiawen Yang, James T Lim, Paul Victor, Marcelo G Corona, Chen Chen, Hunain Khawaja, Qiong Pan, Gillian D Paine-Murrieta, Rick G Schnellmann, Denise J Roe, Prafulla C Gokhale, James A DeCaprio, Megha Padi\",\"doi\":\"10.1101/2023.11.01.565218\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Merkel Cell Carcinoma (MCC) is an aggressive neuroendocrine cutaneous malignancy arising from either ultraviolet-induced mutagenesis or Merkel cell polyomavirus (MCPyV) integration. Despite extensive research, our understanding of the molecular mechanisms driving the transition from normal cells to MCC remains limited. To address this knowledge gap, we assessed the impact of inducible MCPyV T antigens on normal human fibroblasts by performing RNA sequencing. Our data uncovered changes in expression and regulation of Wnt signaling pathway members. Building on this observation, we bioinformatically evaluated various Wnt pathway perturbagens for their ability to reverse the MCC gene expression signature and identified pyrvinium pamoate, an FDA-approved anthelminthic drug known for its anti-tumor activity in other cancers. Leveraging transcriptomic, network, and molecular analyses, we found that pyrvinium targets multiple MCC vulnerabilities. Pyrvinium not only reverses the neuroendocrine features of MCC by modulating canonical and non-canonical Wnt signaling but also inhibits cancer cell growth by activating p53-mediated apoptosis, disrupting mitochondrial function, and inducing endoplasmic reticulum stress. Finally, we demonstrated that pyrvinium reduces tumor growth in an MCC mouse xenograft model. These findings offer a new understanding of the role of Wnt signaling in MCC and highlight the utility of pyrvinium as a potential treatment for MCC.</p>\",\"PeriodicalId\":72407,\"journal\":{\"name\":\"bioRxiv : the preprint server for biology\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-12-20\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10635082/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"bioRxiv : the preprint server for biology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1101/2023.11.01.565218\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"bioRxiv : the preprint server for biology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1101/2023.11.01.565218","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

摘要

梅克尔细胞癌(MCC)是一种高度侵袭性的神经内分泌皮肤恶性肿瘤,由紫外线诱变或梅克尔细胞多瘤病毒(MCPyV)整合引起。它是唯一已知的神经内分泌肿瘤(NET)与病毒病因。尽管进行了广泛的研究,但我们对从正常细胞向MCC转变的分子机制的理解仍然有限。为了解决这一知识空白,我们通过进行RNA测序来评估诱导型MCPyV T抗原对正常人类成纤维细胞的影响。我们的研究结果表明,WNT信号通路在MCC的发展中起着关键作用。为了测试该模型,我们从生物信息学上评估了各种摄动原逆转MCC基因表达特征的能力,并鉴定了pamoate pyrvinium,这是一种经fda批准的抗肿瘤药物,以其在多种癌症中的抗肿瘤潜力而闻名。利用转录组学、网络和分子分析,我们发现pyrvinium有效地针对多个MCC漏洞。具体来说,pyrvinium不仅通过调节典型和非典型WNT信号通路逆转MCC的神经内分泌特征,还通过激活p53介导的凋亡通路、破坏线粒体功能和诱导内质网(ER)应激来抑制癌细胞生长。Pyrvinium还能有效抑制MCC小鼠异种移植模型中的肿瘤生长。这些发现为神经内分泌癌的治疗策略的发展提供了新的途径,并强调了吡啶作为MCC的潜在治疗方法的实用性。意义:我们的研究揭示了WNT信号通路在MCC转化中的作用,并将pamoate pyrvinium描述为一种针对MCC多种脆弱性的有效抗肿瘤试剂。
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
Integrative analysis reveals therapeutic potential of pyrvinium pamoate in Merkel cell carcinoma.

Merkel Cell Carcinoma (MCC) is an aggressive neuroendocrine cutaneous malignancy arising from either ultraviolet-induced mutagenesis or Merkel cell polyomavirus (MCPyV) integration. Despite extensive research, our understanding of the molecular mechanisms driving the transition from normal cells to MCC remains limited. To address this knowledge gap, we assessed the impact of inducible MCPyV T antigens on normal human fibroblasts by performing RNA sequencing. Our data uncovered changes in expression and regulation of Wnt signaling pathway members. Building on this observation, we bioinformatically evaluated various Wnt pathway perturbagens for their ability to reverse the MCC gene expression signature and identified pyrvinium pamoate, an FDA-approved anthelminthic drug known for its anti-tumor activity in other cancers. Leveraging transcriptomic, network, and molecular analyses, we found that pyrvinium targets multiple MCC vulnerabilities. Pyrvinium not only reverses the neuroendocrine features of MCC by modulating canonical and non-canonical Wnt signaling but also inhibits cancer cell growth by activating p53-mediated apoptosis, disrupting mitochondrial function, and inducing endoplasmic reticulum stress. Finally, we demonstrated that pyrvinium reduces tumor growth in an MCC mouse xenograft model. These findings offer a new understanding of the role of Wnt signaling in MCC and highlight the utility of pyrvinium as a potential treatment for MCC.

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
自引率
0.00%
发文量
0
期刊最新文献
Self-supervised segmentation and characterization of fiber bundles in anatomic tracing data. Single neuron contributions to the auditory brainstem EEG. Neural substrates of cold nociception in Drosophila larva. Inversions Can Accumulate Balanced Sexual Antagonism: Evidence from Simulations and Drosophila Experiments. Programming megakaryocytes to produce engineered platelets for delivering non-native proteins.
×
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