Downregulation of circ_0119412 expression inhibits malignant progression of breast cancer by targeting the miR-1205/GALNT6 pathway in vivo and in vitro

Abstract

IntroductionAberrant circular RNA (circRNA) expression is associated with development of breast cancer. In this study, we aimed to assess the anti-proliferative effect of <i>circ_0119412</i> knockdown on breast cancer cells.Material and methodsTumor and adjacent normal tissues were collected from 35 patients with invasive breast cancer (mean age: 56 years; mean tumor size: 2 cm; 46% patients with TNM I and II stages). The levels of <i>circ_0119412</i>, microRNA (<i>miR</i>)-1205, and N-acetylgalactosaminyltransferase 6 (<i>GALNT6</i>) were determined using reverse transcription-quantitative polymerase chain reaction. Cell proliferation and invasion were assessed using cell counting kit-8 and transwell assays, respectively. Cell apoptosis was assessed using flow cytometry. Moreover, the targeting relationships of <i>miR-1205</i> with <i>circ_0119412</i> and <i>GALNT6</i> were determined using dual-luciferase reporter and RNA immunoprecipitation assays. Furthermore, tumor growth was observed in an animal model in vivo.ResultsWe found that <i>circ_0119412</i> expression levels were upregulated in breast cancer tumor specimens and cell lines. Downregulation of <i>circ _0119412</i> inhibited the invasion and proliferation, while enhancing the apoptosis of breast cancer cells. Furthermore, <i>circ_0119412</i> knockdown suppressed tumor growth in vivo. Notably, <i>miR-1205</i> was identified as a downstream target of <i>circ_0119412</i>. Downregulation of <i>circ_0119412</i> suppressed the aggressive behavior of breast cancer cells by targeting <i>miR-1205</i>. Moreover, <i>GALNT6</i> was the downstream target of <i>miR-1205</i>. Inhibition of <i>miR-1205</i> aggravated the malignant behavior of breast cancer cells by increasing <i>GALNT6</i> expression.ConclusionsOur findings suggest that the downregulation of <i>circ_0119412</i> inhibits breast cancer progression, at least in part, by targeting the <i>miR-1205/GALNT6</i> pathway.