{"title":"敲除 PRR11 可通过抑制 Akt/mTOR 信号通路诱导胶质瘤细胞自噬","authors":"Zongxi Li, Lingxuan Ren, Lie Zhang","doi":"10.1134/s1819712424020077","DOIUrl":null,"url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>Glioma is the most common type of primary craniocerebral tumor. Understanding the molecular mechanisms of glioma occurrence and development will provide strategies for effectively treating glioma. Proline-rich protein 11 (PRR11) is a protein which is widely overexpressed in different tumors. TCGA data analysis showed that PRR11 expression was up-regulated in glioma tissues, but its role still needs to be further studied. Here, the role of PRR11 in glioma progression and the mechanism were investigated. We found PRR11 was overexpressed in glioma cells. Depletion of PRR11 suppressed the growth of glioma cells as well as induced cell cycle arrest. We further found PRR11 ablation induced the autophagy of glioma cells. Furthermore, knockdown of PRR11 restrained the activation of Akt/mTOR pathway, thereby suppressing the proliferation of glioma cells. We thought PRR11 could serve as a target for glioma therapy.</p>","PeriodicalId":19119,"journal":{"name":"Neurochemical Journal","volume":null,"pages":null},"PeriodicalIF":0.5000,"publicationDate":"2024-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Knockdown of PRR11 Induces Autophagy in Glioma Cells by Inhibiting Akt/mTOR Signaling Pathway\",\"authors\":\"Zongxi Li, Lingxuan Ren, Lie Zhang\",\"doi\":\"10.1134/s1819712424020077\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<h3 data-test=\\\"abstract-sub-heading\\\">Abstract</h3><p>Glioma is the most common type of primary craniocerebral tumor. Understanding the molecular mechanisms of glioma occurrence and development will provide strategies for effectively treating glioma. Proline-rich protein 11 (PRR11) is a protein which is widely overexpressed in different tumors. TCGA data analysis showed that PRR11 expression was up-regulated in glioma tissues, but its role still needs to be further studied. Here, the role of PRR11 in glioma progression and the mechanism were investigated. We found PRR11 was overexpressed in glioma cells. Depletion of PRR11 suppressed the growth of glioma cells as well as induced cell cycle arrest. We further found PRR11 ablation induced the autophagy of glioma cells. Furthermore, knockdown of PRR11 restrained the activation of Akt/mTOR pathway, thereby suppressing the proliferation of glioma cells. We thought PRR11 could serve as a target for glioma therapy.</p>\",\"PeriodicalId\":19119,\"journal\":{\"name\":\"Neurochemical Journal\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.5000,\"publicationDate\":\"2024-05-27\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Neurochemical Journal\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1134/s1819712424020077\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"NEUROSCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neurochemical Journal","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1134/s1819712424020077","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
Knockdown of PRR11 Induces Autophagy in Glioma Cells by Inhibiting Akt/mTOR Signaling Pathway
Abstract
Glioma is the most common type of primary craniocerebral tumor. Understanding the molecular mechanisms of glioma occurrence and development will provide strategies for effectively treating glioma. Proline-rich protein 11 (PRR11) is a protein which is widely overexpressed in different tumors. TCGA data analysis showed that PRR11 expression was up-regulated in glioma tissues, but its role still needs to be further studied. Here, the role of PRR11 in glioma progression and the mechanism were investigated. We found PRR11 was overexpressed in glioma cells. Depletion of PRR11 suppressed the growth of glioma cells as well as induced cell cycle arrest. We further found PRR11 ablation induced the autophagy of glioma cells. Furthermore, knockdown of PRR11 restrained the activation of Akt/mTOR pathway, thereby suppressing the proliferation of glioma cells. We thought PRR11 could serve as a target for glioma therapy.
期刊介绍:
Neurochemical Journal (Neirokhimiya) provides a source for the communication of the latest findings in all areas of contemporary neurochemistry and other fields of relevance (including molecular biology, biochemistry, physiology, neuroimmunology, pharmacology) in an afford to expand our understanding of the functions of the nervous system. The journal presents papers on functional neurochemistry, nervous system receptors, neurotransmitters, myelin, chromaffin granules and other components of the nervous system, as well as neurophysiological and clinical aspects, behavioral reactions, etc. Relevant topics include structure and function of the nervous system proteins, neuropeptides, nucleic acids, nucleotides, lipids, and other biologically active components.
The journal is devoted to the rapid publication of regular papers containing the results of original research, reviews highlighting major developments in neurochemistry, short communications, new experimental studies that use neurochemical methodology, descriptions of new methods of value for neurochemistry, theoretical material suggesting novel principles and approaches to neurochemical problems, presentations of new hypotheses and significant findings, discussions, chronicles of congresses, meetings, and conferences with short presentations of the most sensational and timely reports, information on the activity of the Russian and International Neurochemical Societies, as well as advertisements of reagents and equipment.