Abstract

To investigate the effects of croton alkaloids on malignant behaviors of breast cancer cells T47D and the possible mechanism. Different doses of croton alkaloids were exposed to T47D cells. T47D cells were transfected with small interfering-circular_0079593 and small interfering-negative control by liposome transfection, respectively. The plasmid cloning deoxyribonucleic acid-circular_0079593 transfected T47D cells were performed with 150 μg/ml croton alkaloids treatment. Circular_0079593 and microRNA-1299 were determined via qualitative reverse transcription polymerase chain reaction in breast cancer samples and cells. 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyl tetrazolium bromide assay and colony formation assay for proliferation, scratch assay for migration and transwell assay for invasion were performed. Circular_0079593 and microRNA-1299 target relationship was examined using dual-luciferase reporter assay. Protein analysis was implemented through Western blot. Croton alkaloids increased cell proliferation inhibition rate and E-cadherin protein level (p<0.05) while reduced colony formation number and invasive cells (p<0.05), and croton alkaloids suppressed scratch healing rate and N-cadherin protein level (p<0.05), and these effects were dose-dependent. Circular_0079593 up-regulation and microRNA-1299 down-regulation were detected in breast cancer tissues contrasted to adjacent samples (p<0.05). Croton alkaloids induced circular_0079593 expression up-regulation (p<0.05) and microRNA-1299 level inhibition (p<0.05) in a dose-dependent manner. Circular_0079593 could targeted regulate the expression of microRNA-1299. Transfection of small interfering-circular_0079593 elevated microRNA-1299 level, and suppressed cell malignant behaviors. Circular_0079593 overexpression could weaken the regulation of croton alkaloids in T47D cell behaviors. Croton alkaloids could repress breast cancer cell proliferation, colony formation, migration and invasion via mediating circ_0079593/microRNA-1299 axis.