Abstract
BackgroundLong intergenic non-protein coding RNA00665 (LINC00665) plays a crucial tumorigenic role in many cancers, such as gastric cancer and lung adenocarcinoma. However, its role and mechanism of action in the progression of breast cancer (BC) are unknown.MethodsLINC00665 expression levels were determined using quantitative polymerase chain reaction analysis with BC tissues and cell lines. BC cell proliferation was tested by performing 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays, whereas BC cell migration and invasion capabilities were analyzed by performing transwell migration assays. Percentages of apoptotic cells were measured by flow cytometry. Interactions between LINC00665 and miR-3169-5p were examined by performing luciferase reporter assays, and the expression levels of proteins, such as β-catenin, were examined by western blot analysis.ResultsLINC00665 was expressed at high levels in BC tissues and cells. Upregulated LINC00665 expression correlated with tumor size and tumor, node, and metastasis stages, but not with the age of patients. LINC00665 knockdown inhibited BC cell proliferation, migration, and invasion, whereas it promoted apoptosis. Moreover, bioinformatics analysis and the luciferase reporter assay revealed that LINC00665 bound the microRNA (miR) miR-3619-5p. miR-3619-5p expression correlated negatively with LINC00665 expression in BC tissues. miR-3619-5p overexpression inhibited BC cell proliferation, migration, and invasion, but promoted apoptosis. Simultaneous knockdown of LINC00665 and miR-3619-5p led to increased cell proliferation, migration, and invasion, and inhibited apoptosis. Additionally, catenin beta 1, which encodes the β-catenin protein, was the target gene of miR-3619-5p. β-catenin expression clearly decreased after LINC00665 knockdown and miR-3619-5p overexpression, but increased after simultaneous knockdown of LINC00665 and miR-3619-5p.ConclusionLINC00665 knockdown inhibited BC cell proliferation and invasion by binding miR-3619-5p and inhibiting β-catenin expression.
Highlights
Long intergenic non-protein coding RNA00665 (LINC00665) plays a crucial tumorigenic role in many cancers, such as gastric cancer and lung adenocarcinoma
Expression of the Long non-coding RNA (lncRNA) colorectal neoplasia differentially expressed is significantly upregulated in breast cancer (BC) cells, where it acts as a competing endogenous RNA and binds miR-136, thereby activating the Wnt/catenin beta 1 (CTNNB1) signaling pathway [9]
LINC00665 was overexpressed in BC tissues The expression profile of the LINC00665 gene was analyzed using the Gene Expression Profiling Interactive Analysis (GEPIA) method with BC and normal tissues
Summary
Long intergenic non-protein coding RNA00665 (LINC00665) plays a crucial tumorigenic role in many cancers, such as gastric cancer and lung adenocarcinoma. Elucidating the role of these genes would significantly help understand the molecular mechanisms underlying BC development, and may reveal specific and reliable markers for developing specific therapeutic interventions. Long non-coding RNAs (lncRNAs) are longer than 200 nucleotides and represent a class of transcripts that are not translated into proteins [3]. LncRNAs play regulatory roles in cell proliferation, apoptosis, invasion, and metastasis in different cancers [4, 5]. One of the regulatory mechanisms involves lncRNAs acting as microRNA (miRNA) sponges by binding miRNAs and thereby modulating the post-transcriptional levels of target miRNAs [6, 7]. The lncRNA myocardial infarction-associated transcript shows significantly higher expression in BC cells than in normal cells, and its knockdown inhibits BC cell proliferation [8]. Exploring the functional roles of novel lncRNAs in BC may help identify new molecular targets for BC treatment
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