Shikonin inhibits migration and invasion of triple-negative breast cancer cells by suppressing epithelial-mesenchymal transition via miR-17-5p/PTEN/Akt pathway

Background: Triple-negative breast cancer (TNBC) is a great threat to global women's health due its high metastatic potential. Epithelial-to-mesenchymal transition (EMT) considered as key event in the process of metastasis. So pharmacological targeting EMT might be promising strategy improving therapeutic efficacy TNBC. Here, we investigated effect shikonin exerting on and consequently metastasis TNBC cells underlying mechanism. Methods: The invasive migratory capacities MDA-MB-231 BT549 were tested using transwell invasion wound healing assay. MiR-17-5p expression was examined by qRT-PCR. targeted genes predicted with different bioinformatic algorithms from four databases (TargetScan, miRanda, PITA picTar) further screened Kyoto Encyclopedia Genes Genomes (KEGG) pathway enrichment analysis. differential expressions their correlations miR-17-5p identified patients based Cancer Genome Atlas (TCGA) database. interaction between phosphatase tensin homolog deleted chromosome ten (PTEN) analyzed luciferase reporter overexpression vector small interfering RNA constructed investigate role PTEN played regulation. markers, protein kinase B (Akt) phospho-Akt (p-Akt) evaluated western blot. Results: Shikonin suppressed migration meanwhile corresponding alterations biomarkers observed treated cells. inhibited miR-17-5p, which upregulated cancer. 3'-untranslated region (3'-UTR) found direct binding target assays. functioned suppressor both Moreover, Akt p-Akt (Ser473) involved inhibition cell migration, shikonin. Conclusions: inhibits suppressing via miR-17-5p/PTEN/Akt pathway. This suggests agent counteract patients.