LncRNA LUCAT1/miR-181a-5p axis promotes proliferation and invasion of breast cancer via targeting KLF6 and KLF15

• Published in: BMC cell biology Vol. 21; no. 1; pp. 1 - 69
• Main Authors: Liu, Yun, Cheng, Teng, Du, Yaying, Hu, Xiaopeng, Xia, Wenfei
• Format: Journal Article
• Language: English
• Published: London BioMed Central Ltd 30.09.2020; BioMed Central; BMC
• Subjects: 3' Untranslated regions; Binding sites; Bioinformatics; Biomarkers; Breast cancer; Cancer invasiveness; Cancer research; Cell adhesion & migration; Cell growth; Cell proliferation; Chromosome 5; Coronary artery disease; Development and progression; Epithelial cells; Gene expression; Genetic aspects; Health aspects; Heart diseases; Kidney diseases; KLF15; KLF6; LUCAT1; Lung cancer; Lung diseases; Medical prognosis; MicroRNAs; miR-181a-5p; mRNA; Non-coding RNA; Radiation therapy; Regulation; RNA; siRNA; Transfection; Tumor suppressor genes; China
• ISSN: 2661-8850; 2661-8850; 1471-2121
• DOI: 10.1186/s12860-020-00310-0

Long non-coding RNAs (lncRNAs) are novel regulatory molecules in breast cancer development. LncRNA LUCAT1 is a potential tumor promoter in human cancers. In this study, we aimed to explore the role of LUCAT1 in human breast cancer tissues and cells. A total of 31 breast cancer patients who underwent tumor resection, but without chemo- or radiotherapy or acute lung/heart/kidney diseases, provided tumor and adjacent normal tissues. Bioinformatic analysis, qRT-PCR, and luciferase reporter assay were carried out during the study. qRT-PCR analysis indicated that, compared with the adjacent tissues and MCF-10A normal breast epithelial cells, LUCAT1 was markedly up-regulated in the breast cancer tissues and five BC cell lines, including MDA-MB-231, MDA-MB-468, MDA-MB-435, SKBR3, and MCF-7. The knockdown of LUCAT1, through the transfection of small interfering RNA (siRNA) specific to LUCAT1, resulted in inhibition of proliferation in breast cancer cells. The expression levels of miR-181a-5p were decreased in the breast cancer tissues and five BC cell lines. Bioinformatic analysis and luciferase reporter assay suggested the interaction between miR-181a-5p and LUCAT1. In addition, the effects of LUCAT1 on promoting cell proliferation were attenuated by overexpression of miR-181a-5p through the transfection of miR-181a-5p mimic. Moreover, bioinformatics and luciferase reporter assay confirmed that miR-181a-5p targeted the 3'-UTR region of KLF6 and KLF15 mRNA, which were two tumor suppressor genes. LUCAT1/miR-181a-5p axis regulated the expression of KLF6 and KLF15 both in vitro and in vivo. Our data indicate that LUCAT1/miR-181a-5p axis can serve as a novel therapeutic target in breast cancer.