| Literature DB >> 31696201 |
Guolei Dong1,2,3,4, Teng Pan5,2,3,4, Dongdong Zhou5,2,3,4, Chunyan Li5,2,3,4, Jingjing Liu5,2,3,4, Jin Zhang5,2,3,4.
Abstract
As the most common cancer and one of the leading causes of cancer-associated mortality, breast cancer continues to need more key molecules to regulate its progression. F-box and leucine-rich repeat protein 19 antisense RNA 1 (known as FBXL19-AS1) is a long non-coding RNA (lncRNA) which has been reported as an oncogene in several types of human cancers. However, the specific downstream targets of FBXL19-AS1 remain unknown. In this study, we set out to find more reliable downstream molecules of FBXL19-AS1 in breast cancer. FBXL19-AS1 was expressed at a high level in breast cancer cells. Loss-of-function experiments revealed that silencing FBXL19-AS1 could impair cell proliferation and induce cell apoptosis in breast cancer. In addition, the location of FBXL19-AS1 in the cytoplasm was detected by fluorescent in situ hybridization assay, while FBXL19-AS1 regulated the expression of Forkhead box M1 (FOXM1) by directly absorbing miR-876-5p. Through rescue assays, it was observed that FOXM1 overexpression recovered the inhibited tumor growth caused by FBXL19-AS1 downregulation. We affirmed the function of FBXL19-AS1 in breast cancer and described the mechanism of the FBXL19-AS1/miR-876-5p/FOXM1 axis. The current work presents the molecular mechanism which underlies FBXL19-AS1 in breast cancer and suggests a comprehensive, feasible FBXL19-AS1-mediated therapeutic approach for treating breast cancer.Entities:
Keywords: FBXL19-AS1; FOXM1; breast cancer; miR-876-5p
Mesh:
Substances:
Year: 2019 PMID: 31696201 DOI: 10.1093/abbs/gmz110
Source DB: PubMed Journal: Acta Biochim Biophys Sin (Shanghai) ISSN: 1672-9145 Impact factor: 3.848