Circular RNA-100219 promotes breast cancer progression by binding to microRNA-485-3p.

Purpose: To investigate whether circ-100219 could promote the proliferation and migration of breast cancer cells by upregulating NTRK3 after binding to microRNA-485-3p, thus participating in the development of breast cancer.

Methods: Breast cancer cell lines MCF-7, MDA-MB-231, MDA-MB-549 and human mammary epithelial cells were cultured. The expression levels of circ-100219, microRNA-485-3p and NTRK3 in breast cancer and paracancer tissues were determined using real-time quantitative polymerase chain reaction (RT-qPCR). The regulatory effects of circ-100219, microRNA-485-3p and NTRK3 on the proliferative and migratory capacities of breast cancer cells were assessed using cell counting kit-8 (CCK-8) and Transwell assay, respectively. Dual-luciferase reporter gene assay was conducted to determine the binding condition among circ-100219, microRNA-485-3p and NTRK3. Rescue experiments were performed in co-transfected breast cancer cells.

Results: RT-qPCR data showed that circ-100219 and NTRK3 were highly expressed, whereas microRNA-485-3p was lowly expressed in breast cancer tissues than those of paracancer tissues. Knockdown of circ-100219 in MCF-7 and MDA-MB-231 cells inhibited their proliferative and migratory capacities. On the contrary, microRNA-485-3p knockdown improved the proliferative and migratory capacities. Dual-luciferase reporter gene assay revealed that circ-100219 could bind to microRNA-485-3p and NTRK3 was the target gene of microRNA-485-3p. Western blot results elucidated that circ-100219 stabilized NTRK3 expression, whereas microRNA-485-3p degraded NTRK3 expression. Rescue experiments demonstrated that overexpression of NTRK3 could partially reverse the inhibited proliferative and migratory capacities induced by circ-100219 knockdown in MCF-7 and MDA-MB-231 cells.

Conclusions: Overexpression of circ-10021 promotes the proliferative and migratory capacities of breast cancer cells by sponging microRNA-485-3p to upregulate the NTRK3 expression.