Fig. 6

Proposed eRNA and NamiRNA interaction in drug resistance (a) and breast cancer tumorigenesis (b). During drug resistance, overexpressed miR-17 represses PTEN leading to the activation of the PI3K-Akt pathway and HIF-1α. Simultaneously, Net1e increases the expression of NET1 while inhibiting the PI3K inhibitor and BCL-2. NET1 and NET1e interact with miR-17 via the PI3K-Akt pathway to inhibit apoptosis and increase tumor growth, while NET1 causes induced drug resistance (a). In breast cancer, fibroblast growth factor receptor 2 interacts with NET1e, the Estrogen receptor (ER), to regulate BRCA and other cancer genes, which are targets of miR-200b ~ 200a ~ 429. These trigger an interaction between miR-200b ~ 200a ~ 429, ER, NET1e, and ER-associated genes leading to tumor suppression, increased proliferation, and inhibited apoptosis in breast cancer cells