{"title":"Acidic Leucine-Rich Nuclear Protein Phosphatase 32B Promotes Prostate Adenocarcinoma Cell Progression by Regulating Apoptosis and Epithelial-Mesenchymal Transition.","authors":"Min A, Lei Wang, Yonghao Xue, Chaoqi Wang","doi":"","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>This work aimed to investigate the expression of acidic leucine-rich nuclear protein phosphatase 32B (ANP32B) in prostate adenocarcinoma (PRAD) and evaluate the effect of ANP32B on the proliferation of prostate adenocarcinoma cells.</p><p><strong>Methods: </strong>We evaluated the expression of ANP32B in PRAD tissues and cells compared to the controls obtained from The Cancer Genome Atlas (TCGA). siRNA targeting ANP32B was transfected into DU145 cells to knockdown the ANP32B expression and plasmids carrying ANP32B coding region were used to overexpress ANP32B in PC3 cells. We analyze the knockdown or overexpression efficiency of ANP32B with quantitative reverse-transcription PCR (RT-qPCR) and Western blot. CCK-8 assay, cell colony formation assay, transwell assay, and EdU labeling were performed to investigate the function of ANP32B on the progression of PRAD. Finally, the expression of the cell cycle marker, apoptosis marker, and epithelial-mesenchymal transition (EMT) marker were detected by Western blot.</p><p><strong>Results: </strong>ANP32B expression was upregulated in PRAD samples compared to normal samples. Exogenous ANP32B overexpression promoted cell viability, cell colony formation, 5-ethynyl-2'-deoxyuridine (EdU) incorporation, and cell migration. Inhibition of ANP32B suppressed cell proliferation, growth, and migration. At the molecular level, the genes promoting cell growth and migration, including cyclin D1 and N-cadherin, were significantly upregulated after ANP32B overexpression, whereas those inhibiting cell growth and migration such as cleaved caspase 3 and E-cadherin were downregulated.</p><p><strong>Conclusion: </strong>The tumor-promoting function of ANP32B can be attributed to its capacity to facilitate cell progression, and it may be considered as a therapeutic marker for PRAD therapy.</p>","PeriodicalId":1,"journal":{"name":"Accounts of Chemical Research","volume":null,"pages":null},"PeriodicalIF":16.4000,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Accounts of Chemical Research","FirstCategoryId":"3","ListUrlMain":"","RegionNum":1,"RegionCategory":"化学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CHEMISTRY, MULTIDISCIPLINARY","Score":null,"Total":0}
引用次数: 0
Abstract
Objective: This work aimed to investigate the expression of acidic leucine-rich nuclear protein phosphatase 32B (ANP32B) in prostate adenocarcinoma (PRAD) and evaluate the effect of ANP32B on the proliferation of prostate adenocarcinoma cells.
Methods: We evaluated the expression of ANP32B in PRAD tissues and cells compared to the controls obtained from The Cancer Genome Atlas (TCGA). siRNA targeting ANP32B was transfected into DU145 cells to knockdown the ANP32B expression and plasmids carrying ANP32B coding region were used to overexpress ANP32B in PC3 cells. We analyze the knockdown or overexpression efficiency of ANP32B with quantitative reverse-transcription PCR (RT-qPCR) and Western blot. CCK-8 assay, cell colony formation assay, transwell assay, and EdU labeling were performed to investigate the function of ANP32B on the progression of PRAD. Finally, the expression of the cell cycle marker, apoptosis marker, and epithelial-mesenchymal transition (EMT) marker were detected by Western blot.
Results: ANP32B expression was upregulated in PRAD samples compared to normal samples. Exogenous ANP32B overexpression promoted cell viability, cell colony formation, 5-ethynyl-2'-deoxyuridine (EdU) incorporation, and cell migration. Inhibition of ANP32B suppressed cell proliferation, growth, and migration. At the molecular level, the genes promoting cell growth and migration, including cyclin D1 and N-cadherin, were significantly upregulated after ANP32B overexpression, whereas those inhibiting cell growth and migration such as cleaved caspase 3 and E-cadherin were downregulated.
Conclusion: The tumor-promoting function of ANP32B can be attributed to its capacity to facilitate cell progression, and it may be considered as a therapeutic marker for PRAD therapy.
研究目的本研究旨在调查酸性富亮氨酸核蛋白磷酸酶32B（ANP32B）在前列腺癌（PRAD）中的表达，并评估ANP32B对前列腺癌细胞增殖的影响：将靶向ANP32B的siRNA转染至DU145细胞以敲除ANP32B的表达，并使用携带ANP32B编码区的质粒在PC3细胞中过表达ANP32B。我们通过逆转录定量 PCR（RT-qPCR）和 Western 印迹来分析 ANP32B 的敲除或过表达效率。通过CCK-8检测、细胞集落形成检测、Transwell检测和EdU标记来研究ANP32B对PRAD进展的作用。最后，通过 Western blot 检测细胞周期标志物、细胞凋亡标志物和上皮-间质转化（EMT）标志物的表达：结果：与正常样本相比，ANP32B在PRAD样本中表达上调。外源性ANP32B过表达可促进细胞活力、细胞集落形成、5-乙炔基-2'-脱氧尿苷（EdU）掺入和细胞迁移。抑制 ANP32B 可抑制细胞增殖、生长和迁移。在分子水平上，ANP32B过表达后，促进细胞生长和迁移的基因（包括细胞周期蛋白D1和N-cadherin）显著上调，而抑制细胞生长和迁移的基因（如裂解的caspase 3和E-cadherin）则下调：结论：ANP32B的肿瘤促进功能可归因于其促进细胞进展的能力，它可被视为PRAD治疗的治疗标志物。
期刊介绍：
Accounts of Chemical Research presents short, concise and critical articles offering easy-to-read overviews of basic research and applications in all areas of chemistry and biochemistry. These short reviews focus on research from the author’s own laboratory and are designed to teach the reader about a research project. In addition, Accounts of Chemical Research publishes commentaries that give an informed opinion on a current research problem. Special Issues online are devoted to a single topic of unusual activity and significance.
Accounts of Chemical Research replaces the traditional article abstract with an article "Conspectus." These entries synopsize the research affording the reader a closer look at the content and significance of an article. Through this provision of a more detailed description of the article contents, the Conspectus enhances the article's discoverability by search engines and the exposure for the research.
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