Ziye Wang, Xiaoguang Li, Zhengdao Liu, Yang Du, Tao Wu
{"title":"LncRNA HANR promotes the aerobic glycolysis in prostate cancer by stabilizing TPI1","authors":"Ziye Wang, Xiaoguang Li, Zhengdao Liu, Yang Du, Tao Wu","doi":"10.1016/j.yexcr.2025.114744","DOIUrl":null,"url":null,"abstract":"<div><div>Prostate cancer (PCa) is a type of malignancy that originates in the prostate gland, often characterized by uncontrolled cell growth and potential metastasis. Long non-coding RNAs (lncRNAs) play crucial regulatory roles in the progression of prostate cancer, potentially facilitating tumor growth and metastasis via mechanisms that involve the enhancement of aerobic glycolysis. This study aimed to investigate the functional role of lncRNA HANR in prostate cancer progression. Bioinformatics analysis and experimental validation revealed a significant up-regalation of HANR in prostate cancer tissues, in comparison to adjacent normal tissues. Functional studies demonstrated that silencing HANR inhibited prostate cancer cells proliferation, migration, invasion, and glycolysis. While HANR overexpression promoted prostate cancer cells proliferation, invasion, and glycolysis. Mechanistically, HANR interacts with triosephosphate isomerase 1 (TPI1), a key glycolytic enzyme, to promote glycolysis and tumor growth. Silencing HANR or TPI1 reduced prostate tumor growth both <em>in vitro</em> and <em>in vivo</em>. In conclusion, our findings suggest that the HANR-TPI1 axis plays a crucial role in the progression of prostate cancer and may represent a novel biomarker and therapeutic target for aggressive prostate cancer, given its role in enhancing aerobic glycolysis and facilitating tumorigenesis in prostate cancer cells.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"452 1","pages":"Article 114744"},"PeriodicalIF":3.5000,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Experimental cell research","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0014482725003441","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Prostate cancer (PCa) is a type of malignancy that originates in the prostate gland, often characterized by uncontrolled cell growth and potential metastasis. Long non-coding RNAs (lncRNAs) play crucial regulatory roles in the progression of prostate cancer, potentially facilitating tumor growth and metastasis via mechanisms that involve the enhancement of aerobic glycolysis. This study aimed to investigate the functional role of lncRNA HANR in prostate cancer progression. Bioinformatics analysis and experimental validation revealed a significant up-regalation of HANR in prostate cancer tissues, in comparison to adjacent normal tissues. Functional studies demonstrated that silencing HANR inhibited prostate cancer cells proliferation, migration, invasion, and glycolysis. While HANR overexpression promoted prostate cancer cells proliferation, invasion, and glycolysis. Mechanistically, HANR interacts with triosephosphate isomerase 1 (TPI1), a key glycolytic enzyme, to promote glycolysis and tumor growth. Silencing HANR or TPI1 reduced prostate tumor growth both in vitro and in vivo. In conclusion, our findings suggest that the HANR-TPI1 axis plays a crucial role in the progression of prostate cancer and may represent a novel biomarker and therapeutic target for aggressive prostate cancer, given its role in enhancing aerobic glycolysis and facilitating tumorigenesis in prostate cancer cells.
期刊介绍:
Our scope includes but is not limited to areas such as: Chromosome biology; Chromatin and epigenetics; DNA repair; Gene regulation; Nuclear import-export; RNA processing; Non-coding RNAs; Organelle biology; The cytoskeleton; Intracellular trafficking; Cell-cell and cell-matrix interactions; Cell motility and migration; Cell proliferation; Cellular differentiation; Signal transduction; Programmed cell death.