Fig 2: The underlying mechanism of apoptosis and G2/M arrest was determined by ROS assay and ELISA. The apoptotic cell-induced effects of helenalin, BHM, and BHG were detected by increasing ROS levels (a) and p53 expression (b). Helenalin, BHM, and BHG suppressed STAT3-MYC-CDC25-CDK1 signaling and increased p21 to induce G2/M arrest in MDA-MB-231 cells (c–f). * represented p < 0.05 as compared to untreated control. Each data is expressed as the mean ± standard error of at least two experiments, each performed in duplicate.

Fig 3: Bioinformatics analysis of the expression of MYC and its regulating pathway in the TNBC patients. (a) The oncoprint analysis of MYC amplification or mRNA upregulation in the TNBC cohort and non-TNBC cohort from TCGA and METABRIC breast cancer datasets. (b) MYC mRNA expression was detected in breast cancer according to the 3-gene classifier subtype. (c) The oncoprint analysis of STAT3, MYC, CDC25, and CDK1 in the TNBC cohort and non-TNBC cohort from METABRIC breast cancer datasets. (d) Kaplan–Meier survival analysis of patients with alterations in query genes. (e) Pearson’s correlation of STAT3 and MYC expression in the TNBC cohort.