{"title":"HDAC1 介导的 NEU1 下调会加剧宫颈癌的侵袭性","authors":"Nanzi Xie, Sisi Mei, Changlan Dai, Wei Chen","doi":"10.1615/critreveukaryotgeneexpr.2023051396","DOIUrl":null,"url":null,"abstract":"HDAC1 functions as an oncogene in multi-type cancers. This study aimed to investigate the roles of HDAC1 in cervical cancer (CC). mRNA expression was determined using RT-PCR. Mitochondrial energy metabolism and oxidative stress in clinical samples were determined using corresponding kits. The protein–protein complexes was analyzed using Co-IP assay. The binding sites between NRF2 and NEU1 were confirmed by ChIP assay. Cell viability was detected by CCK-8. Cell proliferation was measured using CCK-8 and colony formation assays. Cell migrative and invasive ability were determined using transwell assay. We found that HDAC1 was upregulated in CC. TSA treatment suppressed mitochondrial energy metabolism, as well as decreased the number of colonies and migrated and invaded cells. Moreover, HDAC1 interacted with NRF2 to downregulate NEU1 expression. NEU1 knockdown attenuated the effects of TSA and enhanced the aggressiveness of CC cells. In conclusion, HDAC1 functions as an oncogene in CC. Targeting HDAC1 may be an alternative strategy for CC.","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":null,"pages":null},"PeriodicalIF":1.5000,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"HDAC1-mediated downregulation of NEU1 exacerbates the aggressiveness of cervical cancer\",\"authors\":\"Nanzi Xie, Sisi Mei, Changlan Dai, Wei Chen\",\"doi\":\"10.1615/critreveukaryotgeneexpr.2023051396\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"HDAC1 functions as an oncogene in multi-type cancers. This study aimed to investigate the roles of HDAC1 in cervical cancer (CC). mRNA expression was determined using RT-PCR. Mitochondrial energy metabolism and oxidative stress in clinical samples were determined using corresponding kits. The protein–protein complexes was analyzed using Co-IP assay. The binding sites between NRF2 and NEU1 were confirmed by ChIP assay. Cell viability was detected by CCK-8. Cell proliferation was measured using CCK-8 and colony formation assays. Cell migrative and invasive ability were determined using transwell assay. We found that HDAC1 was upregulated in CC. TSA treatment suppressed mitochondrial energy metabolism, as well as decreased the number of colonies and migrated and invaded cells. Moreover, HDAC1 interacted with NRF2 to downregulate NEU1 expression. NEU1 knockdown attenuated the effects of TSA and enhanced the aggressiveness of CC cells. In conclusion, HDAC1 functions as an oncogene in CC. Targeting HDAC1 may be an alternative strategy for CC.\",\"PeriodicalId\":56317,\"journal\":{\"name\":\"Critical Reviews in Eukaryotic Gene Expression\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":1.5000,\"publicationDate\":\"2024-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Critical Reviews in Eukaryotic Gene Expression\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1615/critreveukaryotgeneexpr.2023051396\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"BIOTECHNOLOGY & APPLIED MICROBIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Critical Reviews in Eukaryotic Gene Expression","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1615/critreveukaryotgeneexpr.2023051396","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOTECHNOLOGY & APPLIED MICROBIOLOGY","Score":null,"Total":0}
HDAC1-mediated downregulation of NEU1 exacerbates the aggressiveness of cervical cancer
HDAC1 functions as an oncogene in multi-type cancers. This study aimed to investigate the roles of HDAC1 in cervical cancer (CC). mRNA expression was determined using RT-PCR. Mitochondrial energy metabolism and oxidative stress in clinical samples were determined using corresponding kits. The protein–protein complexes was analyzed using Co-IP assay. The binding sites between NRF2 and NEU1 were confirmed by ChIP assay. Cell viability was detected by CCK-8. Cell proliferation was measured using CCK-8 and colony formation assays. Cell migrative and invasive ability were determined using transwell assay. We found that HDAC1 was upregulated in CC. TSA treatment suppressed mitochondrial energy metabolism, as well as decreased the number of colonies and migrated and invaded cells. Moreover, HDAC1 interacted with NRF2 to downregulate NEU1 expression. NEU1 knockdown attenuated the effects of TSA and enhanced the aggressiveness of CC cells. In conclusion, HDAC1 functions as an oncogene in CC. Targeting HDAC1 may be an alternative strategy for CC.
期刊介绍:
Critical ReviewsTM in Eukaryotic Gene Expression presents timely concepts and experimental approaches that are contributing to rapid advances in our mechanistic understanding of gene regulation, organization, and structure within the contexts of biological control and the diagnosis/treatment of disease. The journal provides in-depth critical reviews, on well-defined topics of immediate interest, written by recognized specialists in the field. Extensive literature citations provide a comprehensive information resource.
Reviews are developed from an historical perspective and suggest directions that can be anticipated. Strengths as well as limitations of methodologies and experimental strategies are considered.