| Literature DB >> 31215650 |
Yue-Yue Wang1,2, Lei Yan1, Shuo Yang1, He-Nan Xu1, Tian-Tian Chen1, Zheng-Yuan Dong1, Su-Lian Chen1,3, Wen-Rui Wang1,4, Qing-Ling Yang1,3, Chang-Jie Chen1,3.
Abstract
Breast cancer (BC) is the most prevalent malignant cancer in the world, is the leading cause of cancer-related death female. Recently, there is accumulating evidence that long noncoding RNAs (lncRNAs) might as an important role in the progression of BC. (epithelial-mesenchymal transition (EMT) is considered to play a vital role in tumor cells migration and invasion. Nevertheless, the entire biological mechanisms and functions of lncRNAs in tumor migration, invasion, and EMT remain uncertain. In the present research, we observed that the expression of lncRNA AC073284.4 was downregulated in BC paclitaxel-resistant (PR) cells (MCF-7/PR) and tissues. Bioinformatics analysis predicted that miR-18b-5p was a direct target of AC073284.4, which has been validated by dual-luciferase reporter gene assay. We further proved that AC073284.4 could directly bind to miR-18b-5p and relieve the suppression for dedicator of cytokinesis protein 4 (DOCK4). Furthermore, the underlying functional experiments demonstrated that AC073284.4 might sponge miR-18b-5p to attenuate the invasion, metastasis, and EMT of BC cell through upregulating DOCK4 expression. In summary, AC073284.4 might serve as a competing endogenous RNA (ceRNA) in BC progression via modulating miR-18b-5p/DOCK4 axis, which weakens EMT and migration of BC. These results suggesting that AC073284.4 might function as a potential novel diagnostic biomarker in the progression of BC.Entities:
Keywords: AC073284.4; DOCK4; EMT; breast cancer; miR-18b-5p
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Year: 2019 PMID: 31215650 DOI: 10.1002/jcp.28887
Source DB: PubMed Journal: J Cell Physiol ISSN: 0021-9541 Impact factor: 6.384