Role of long-chain non-coding ribonucleic acid (lncRNA) GACAT1 in the development of breast cancer and its possible mechanism were investigated. The levels of GACAT1, microRNA-875-3p and Stonin2 (STON2) in breast cancer tissues and adjacent normal tissues were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The level of GACAT1 in breast cancer cell lines was further explored. The effects of GACAT1 and microRNA-875-3p on cell proliferation and cycle were detected by cell counting kit-8 (CCK-8) and flow cytometry. The binding relationship between microRNA-875-3p and STON2, microRNA-875-3p and GACAT1 was examined by a dual luciferase reporting assay. It was confirmed by rescue experiments whether GACAT1 canregulate the level of STON2 by binding to microRNA-875-3p. GACAT1 level was clearly enhanced in breast cancer tissues compared to that of the adjacent tissues. Similar result was observed in breast cancer cell lines. Upregulation of GACAT1 promoted the proliferation and cycle of breast cancer cells including MCF-7 and BCap-37. The dual luciferase reporting assay results indicated that GACAT1 had a binding relationship with microRNA-875-3p. Further experiments confirmed that microRNA-875-3p was conspicuously downregulated in breast cancer tissues, and upregulation of microRNA-875-3p could inhibit the proliferation ability of MCF-7 and BCap-37 cells, and partially reversed the promoting effect of GACAT1 on cell cycle. Through bioinformatics prediction and dual luciferase reporter gene experiments, we found that STON2 might be a target gene of microRNA-875-3p. Overexpression of STON2 could partially abolish the effect of microRNA-875-3p on cell proliferation and cycle of MCF-7 and BCap-37 cells. GACAT1 can participate in the progression of breast cancer by promoting the proliferation and cycle of breast cancer cells. The mechanism may be through the regulation of the level of STON2 by adsorbing microRNA-875-3p.

Breast cancer (BC) is one of the most common fatal cancers. Recent studies have identified the vital role of long non-coding RNAs (lncRNAs) in the development and progression of BC. In this investigation, lncRNA TTN-AS1 was studied to identify its function in the metastasis of BC. TTN-AS1 expression of tissues was detected by real-time quantitative polymerase chain reaction (RT-qPCR) in 56 BC patients. Wound healing assay and transwell assay were used to observe the biological behavior changes of BC cells through gain or loss of TTN-AS1. In addition, luciferase assays and RNA immunoprecipitation (RIP) assay were performed to discover the potential targets of TTN-AS1 in BC cells. TTN-AS1 expression level in BC samples was higher than that of adjacent tissue. Besides, the ability of cell migration and invasion of BC cells was inhibited after TTN-AS1 was silenced, while cell migration and cell invasion of BC cells were promoted after TTN-AS1 was overexpressed. In addition, miR-140-5p was upregulated after silencing of TTN-AS1 in BC cells, while miR-140-5p was downregulated after overexpression of TTN-AS1 in BC cells. Furthermore, luciferase assays and RIP assay showed that miR-140-5p was a direct target of TTN-AS1 in BC. Our study uncovered a new oncogene in BC and suggests that TTN-AS1 enhances BC cell migration and invasion via sponging miR-140-5p, which provides a novel therapeutic target for BC patients.

Long non-coding RNA TTN-AS1 promotes breast cancer cell migration and invasion via sponging miR-140-5p JIE XUE, ZHIXIA ZHANG, XIAONA LI, QINGFANG REN and QINGHUA WANG This work is licensed under a Creative Commons Attribution 4.0 International (CC BY 4.0) License.