Long non‑coding RNA DANCR aggravates breast cancer through the miR‑34c/E2F1 feedback loop

Abstract

Emerging scientific evidence has suggested that the long non‑coding (lnc)RNA differentiation antagonizing non‑protein coding RNA (DANCR) serves a significant role in human tumorigenesis and cancer progression; however, the precise mechanism of its function in breast cancer remains to be fully understood. Therefore, the objective of the present study was to manipulate DANCR expression in MCF7 and MDA‑MB‑231 cells using lentiviral vectors to knock down or overexpress DANCR. This manipulation, alongside the anal‑ ysis of bioinformatics data, was performed to investigate the potential mechanism underlying the role of DANCR in cancer. The mRNA and/or protein expression levels of DANCR, miR‑34c‑5pandE2Ftranscriptionfactor1(E2F1)wereassessed using reverse transcription‑quantitative PCR and western blot‑ ting, respectively. The interactions between these molecules were validated using chromatin immunoprecipitation and dual‑luciferase reporter assays. Additionally, fluorescence in situ hybridization was used to confirm the subcellular localization of DANCR. Cell proliferation, migration and invasion were determined using 5‑ethynyl‑2'‑deoxyuridine, wound healing and Transwell assays, respectively. The results of the present study demonstrated that DANCR had a regula‑ tory role as a competing endogenous RNA and upregulated the expression of E2F1 by sequestering miR‑34c‑5p in breast cancer cells. Furthermore, E2F1 promoted DANCR transcrip‑ tion by binding to its promoter in breast cancer cells. Notably, the DANCR/miR‑34c‑5p/E2F1 feedback loop enhanced cell