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http://purl.uniprot.org/citations/34403101http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/34403101http://www.w3.org/2000/01/rdf-schema#comment"

Objective

The expression levels of histone deacetylase 2 (HDAC2), eukaryotic initiation factor 5 (eIF5), and eukaryotic initiation factor 6 (eIF6), and relationship between HDAC2 and eIF5 or eIF6 in lung cancer tissues were investigated, in order to charify the relationship between HDAC2 and the prognosis of lung cancer patients and its influence on the expression of eIF5 and eIF6.

Methods

The expression of HDAC2, eIF5, and eIF6 in lung cancer tissues was detected by quantitative reverse transcription polymerase chain reaction. The expression correlation between HDAC2 and eIF5 or eIF6 was tested using a t test. The correlation between HDAC2 and eIF5 or eIF6 was analyzed using the TCGA database. The identified cells were constructed with small interfering siRNA and HDAC2 overexpression plasmid. The proliferation and migration ability of the identified cells was investigated by CCK8 and Transwell assays, respectively.

Results

HDAC2, eIF5, and eIF6 were overexpressed in lung cancer tissues, and HDAC2 expression level was negatively correlated with the prognosis of lung cancer patients. HDAC2 expression level was positively correlated with eIF5 and eIF6 expression levels. HDAC2 could regulate the expression of eIF5 and eIF6. The regulation of proliferation and invasion of lung cancer cells by HDAC2 depended on eIF5 and eIF6.

Conclusion

HDAC2, eIF5, and eIF6 were closely related with lung cancer tumorigenesis, which might be potential biological markers and therapeutic targets for lung cancer."xsd:string
http://purl.uniprot.org/citations/34403101http://purl.org/dc/terms/identifier"doi:10.1007/s11596-021-2389-z"xsd:string
http://purl.uniprot.org/citations/34403101http://purl.uniprot.org/core/author"Zeng W."xsd:string
http://purl.uniprot.org/citations/34403101http://purl.uniprot.org/core/author"Chen W.S."xsd:string
http://purl.uniprot.org/citations/34403101http://purl.uniprot.org/core/author"Wang J.S."xsd:string
http://purl.uniprot.org/citations/34403101http://purl.uniprot.org/core/author"Cheng X.F."xsd:string
http://purl.uniprot.org/citations/34403101http://purl.uniprot.org/core/author"Cai S.X."xsd:string
http://purl.uniprot.org/citations/34403101http://purl.uniprot.org/core/author"Lin M.B."xsd:string
http://purl.uniprot.org/citations/34403101http://purl.uniprot.org/core/date"2021"xsd:gYear
http://purl.uniprot.org/citations/34403101http://purl.uniprot.org/core/name"Curr Med Sci"xsd:string
http://purl.uniprot.org/citations/34403101http://purl.uniprot.org/core/pages"764-769"xsd:string
http://purl.uniprot.org/citations/34403101http://purl.uniprot.org/core/title"Roles of HDAC2, eIF5, and eIF6 in Lung Cancer Tumorigenesis."xsd:string
http://purl.uniprot.org/citations/34403101http://purl.uniprot.org/core/volume"41"xsd:string
http://purl.uniprot.org/citations/34403101http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/34403101
http://purl.uniprot.org/citations/34403101http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/34403101
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