<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>55(12)</volume><submitter>Zhu Y</submitter><pubmed_abstract>Krüppel-like zinc-finger transcription factor 5 (KLF5) is a vital regulator of breast cancer (BC) onset and progression. The mechanism by which KLF5 regulates BC is still not clearly known. In this study, bioinformatics analysis shows that BC-affected individuals with elevated KLF5 expression levels have poor clinical outcomes. We further verify that miR-145-5p regulated KLF5 expression to promote cell apoptosis and inhibit cell proliferation in BC via dual-luciferase reporter assay, western blot analysis, qRT-PCR, CCK-8 assay and cell apoptosis assay. In addition, based on bioinformatics analysis, the binding of ENST00000422059 with miR-145-5p is confirmed by dual-luciferase reporter assay. Subsequently, FISH, western blot analysis, qRT-PCR, CCK-8 and cell apoptosis assays verified that E</pubmed_abstract><journal>Acta biochimica et biophysica Sinica</journal><pagination>1892-1901</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10753370</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>lncRNA ENST00000422059 promotes cell proliferation and inhibits cell apoptosis in breast cancer by regulating the miR-145-5p/KLF5 axis.</pubmed_title><pmcid>PMC10753370</pmcid><pubmed_authors>Jiang Y</pubmed_authors><pubmed_authors>Li Y</pubmed_authors><pubmed_authors>Zhu Y</pubmed_authors><pubmed_authors>Ren J</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Wang Y</pubmed_authors><pubmed_authors>Xu J</pubmed_authors><pubmed_authors>Wu X</pubmed_authors><pubmed_authors>Tan Q</pubmed_authors></additional><is_claimable>false</is_claimable><name>lncRNA ENST00000422059 promotes cell proliferation and inhibits cell apoptosis in breast cancer by regulating the miR-145-5p/KLF5 axis.</name><description>Krüppel-like zinc-finger transcription factor 5 (KLF5) is a vital regulator of breast cancer (BC) onset and progression. The mechanism by which KLF5 regulates BC is still not clearly known. In this study, bioinformatics analysis shows that BC-affected individuals with elevated KLF5 expression levels have poor clinical outcomes. We further verify that miR-145-5p regulated KLF5 expression to promote cell apoptosis and inhibit cell proliferation in BC via dual-luciferase reporter assay, western blot analysis, qRT-PCR, CCK-8 assay and cell apoptosis assay. In addition, based on bioinformatics analysis, the binding of ENST00000422059 with miR-145-5p is confirmed by dual-luciferase reporter assay. Subsequently, FISH, western blot analysis, qRT-PCR, CCK-8 and cell apoptosis assays verified that E</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Nov</publication><modification>2025-04-26T07:00:29.48Z</modification><creation>2025-04-06T12:04:46.5Z</creation></dates><accession>S-EPMC10753370</accession><cross_references><pubmed>37997376</pubmed><doi>10.3724/abbs.2023226</doi></cross_references></HashMap>