PUS7 promotes the progression of pancreatic cancer by interacting ANLN to activate MYC pathway.

IF 3.5 2区生物学 Q3 CELL BIOLOGY

Molecular and Cellular Biochemistry Pub Date : 2025-07-01 Epub Date: 2025-04-01 DOI:10.1007/s11010-025-05267-2

Yubo Jiang, Qian Cheng, Yingying Zhang, Jingtao Zhong

{"title":"PUS7 promotes the progression of pancreatic cancer by interacting ANLN to activate MYC pathway.","authors":"Yubo Jiang, Qian Cheng, Yingying Zhang, Jingtao Zhong","doi":"10.1007/s11010-025-05267-2","DOIUrl":null,"url":null,"abstract":"<p><p>To investigate the role of pseudouridine synthase 7 (PUS7) in pancreatic cancer (PC) and explore its underlying molecular mechanisms. PUS7 role in the malignant biological function of PC cells was investigated by colony formation, EdU, flow cytometry, and transwell assays. PUS7 function on glycolysis of PC cells was determined through assessing the extracellular acidification rate and oxygen consumption rate. Besides, the potential molecular mechanism by which PUS7 affects PC was investigated via utilizing immunohistochemistry staining, western blot, qRT-PCR, and co-immunoprecipitation. Xenograft tumors were constructed using BALB/c nude mice. PUS7 was highly expressed in PC tissues. PUS7 significantly accelerated proliferation, mobility and glycolysis, but suppressed apoptosis in PC. Furthermore, PUS7 promoted the malignant biological function of PC cells by interacting anillin (ANLN). We also demonstrated that PUS7 promoted the malignant biological function of PC cells by activating the MYC pathway. PUS7 promoted PC progression via activating the MYC pathway in vivo. Our results indicated that PUS7 could promote cell proliferation, mobility and glycolysis, and inhibit apoptosis by interacting ANLN to activate the MYC pathway in PC.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4401-4415"},"PeriodicalIF":3.5000,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular and Cellular Biochemistry","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1007/s11010-025-05267-2","RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/4/1 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"CELL BIOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

To investigate the role of pseudouridine synthase 7 (PUS7) in pancreatic cancer (PC) and explore its underlying molecular mechanisms. PUS7 role in the malignant biological function of PC cells was investigated by colony formation, EdU, flow cytometry, and transwell assays. PUS7 function on glycolysis of PC cells was determined through assessing the extracellular acidification rate and oxygen consumption rate. Besides, the potential molecular mechanism by which PUS7 affects PC was investigated via utilizing immunohistochemistry staining, western blot, qRT-PCR, and co-immunoprecipitation. Xenograft tumors were constructed using BALB/c nude mice. PUS7 was highly expressed in PC tissues. PUS7 significantly accelerated proliferation, mobility and glycolysis, but suppressed apoptosis in PC. Furthermore, PUS7 promoted the malignant biological function of PC cells by interacting anillin (ANLN). We also demonstrated that PUS7 promoted the malignant biological function of PC cells by activating the MYC pathway. PUS7 promoted PC progression via activating the MYC pathway in vivo. Our results indicated that PUS7 could promote cell proliferation, mobility and glycolysis, and inhibit apoptosis by interacting ANLN to activate the MYC pathway in PC.

查看原文本刊更多论文

PUS7通过与ANLN相互作用激活MYC通路促进胰腺癌的进展。

目的探讨假尿嘧啶合成酶7 （PUS7）在胰腺癌（PC）中的作用及其分子机制。通过集落形成、EdU、流式细胞术和transwell实验研究PUS7在PC细胞恶性生物学功能中的作用。通过测定细胞外酸化速率和耗氧速率来确定PUS7对PC细胞糖酵解的作用。通过免疫组织化学染色、western blot、qRT-PCR、共免疫沉淀等方法研究PUS7影响PC的潜在分子机制。用BALB/c裸鼠构建异种移植瘤。PUS7在PC组织中高表达。PUS7显著促进PC细胞的增殖、迁移和糖酵解，但抑制细胞凋亡。此外，PUS7通过相互作用anillin （ANLN）促进PC细胞的恶性生物学功能。我们还证明了PUS7通过激活MYC通路促进PC细胞的恶性生物学功能。在体内，PUS7通过激活MYC通路促进PC进展。结果表明，PUS7通过与ANLN相互作用激活PC细胞MYC通路，促进细胞增殖、迁移和糖酵解，抑制细胞凋亡。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Molecular and Cellular Biochemistry 生物-细胞生物学

CiteScore

8.30

自引率

2.30%

发文量

293

审稿时长

1.7 months

期刊介绍： Molecular and Cellular Biochemistry: An International Journal for Chemical Biology in Health and Disease publishes original research papers and short communications in all areas of the biochemical sciences, emphasizing novel findings relevant to the biochemical basis of cellular function and disease processes, as well as the mechanics of action of hormones and chemical agents. Coverage includes membrane transport, receptor mechanism, immune response, secretory processes, and cytoskeletal function, as well as biochemical structure-function relationships in the cell. In addition to the reports of original research, the journal publishes state of the art reviews. Specific subjects covered by Molecular and Cellular Biochemistry include cellular metabolism, cellular pathophysiology, enzymology, ion transport, lipid biochemistry, membrane biochemistry, molecular biology, nuclear structure and function, and protein chemistry.