Objective To investigate the specific effect and clinical mechanism of circ_0000212 on proliferation and apoptosis of triple negative breast cancer (TNBC) MDA-MB-231 cells.

Methods Forty-one patients with TNBC diagnosed by pathology and with complete relevant information were selected as the research objects, and their excised cancer tissue and paracancer tissue were taken. The expression levels of circ_0000212 and microRNA(miRNA)-1283 in cancer tissues and adjacent tissues were detected by real-time reverse transcription quantitative polymerase chain reaction (RT-qPCR). MDA-MB-231 cells were randomly divided into si-circ_0000212 group, si-NC group, miR-1283 group, miR-NC group, si-circ_0000212+anti-miR-1283 group, si-circ_0000212+anti-miR-NC group; CCK-8 was used to detect MDA-MB-231 cell viability; clone formation experiment was used to detect MDA-MB-231 cell clone formation number; cell apoptosis rate was detected by flow cytometry; western blot used to detect apoptosis-related protein expression; dual luciferase reporter experiment was used to detect and validate the targeting relationship between circ_0000212 and miR-1283.

Results The expression level of circ_0000212 in the TNBC tissues was higher than that in the para-cancer tissues, and the expression level of miR-128 was significantly lower than that in the para-cancer tissues (P < 0.05). After interference with circ_0000212 expression or miR-128 overexpression, MDA-MB-231 cell viability and clone activity decreased (P < 0.05); the apoptosis rate of MDA-MB-231 cells and the expression level of cleaved-caspase3 and cleaved-caspase9 protein in the si-circ_0000212 group were significantly higher than those in the si-NC group (P < 0.05); the apoptosis rate of MDA-MB-231 cells and the expression level of cleaved-caspase3 and cleaved-caspase9 in the miR-1283 group were significantly higher than those in the miR-NC (P < 0.05).

Conclusion Interfering with the expression of circ_0000212 may inhibit the proliferation of TNBC MDA-MB-231 cells and promote cell apoptosis by targeting up-regulation of miR-1283.