lnc‑MICAL2‑1 sponges miR‑25 to regulate DKK3 expression and inhibits activation of the Wnt/β‑catenin signaling pathway in breast cancer

• DOI: 10.3892/ijmm.2021.5078
• Publication Date: 2021-12-30T10:35:53Z
• Authors: Jia Yao; Guanqiao Li; Minfeng Liu; Shiping Yang; Huiluan Su; Changsheng Ye
• Keywords: 0301 basic medicine; Mice, Inbred BALB C; Transcription, Genetic; Down-Regulation; Mice, Nude; Breast Neoplasms; Up-Regulation; 3. Good health; Gene Expression Regulation, Neoplastic; MicroRNAs; Mice; 03 medical and health sciences; Cell Movement; Cell Line, Tumor; Animals; Humans; Female; Neoplasm Invasiveness; RNA, Long Noncoding; Wnt Signaling Pathway; Adaptor Proteins, Signal Transducing; Cell Proliferation

The Dickkopf 3 (DKK3) protein antagonizes the Wnt receptor complex in signaling pathway; however, to date, there have been no relevant studies investigating its upstream regulatory mechanism breast cancer (BC), best of our knowledge. present study aimed explore whether long non‑coding RNA MICAL2‑1 (lnc‑MICAL2‑1) sponged microRNA (miR)‑25 regulate DKK3 and inhibit activation Wnt/β‑catenin pathway. Atlas Cancer database was used measure expression levels lnc‑MICAL2‑1 their correlation with levels. In addition, cell proliferation, invasion migration were determined following silencing or overexpression lnc‑MICAL2‑1. binding between miR‑25, miR‑25 verified using pull‑down dual‑luciferase reporter assays. effects knockdown on pathway further evaluated a nude mouse xenograft model. results revealed that, compared adjacent normal tissue, downregulated BC tissues, found be positively correlated expression. cells upregulated mRNA inhibited proliferation. Results from dual luciferase assays validated that could bind which targets DKK3. <em>in vivo</em> experimental data demonstrated tumor growth via regulating conclusion, findings highlighted novel molecular through may DKK3‑mediated BC, highlighting potential for treatment disease.