| Expression pattern: |
UP |
| Associated gene: |
HK2, Ago2 |
| Associated microRNA: |
miR-1286 |
| Biological function: |
promotes paclitaxel resistance and malignant behaviors; its silencing sensitizes PTX-resistant BC cells to PTX, suppresses colony formation and cell cycle progression, promotes apoptosis, and reduces glycolysis-related phenotypes. |
| Molecular mechanism: |
circHIPK3 directly binds miR-1286 and modulates HK2 expression through miR-1286, affecting PTX sensitivity and glycolysis-associated phenotypes. |
| Biological pathway or process: |
chemoresistance (inhibits); glycolysis (inhibits); apoptosis (promotes); cell cycle (inhibits); proliferation (inhibits); ceRNA regulation (promotes) |
| Detected method: |
Q
|
| Validation methods: |
RT-qPCR; RNase R Treatment; Nuclear-Cytoplasmic Fractionation; Luciferase Reporter Assay; RIP (RNA Immunoprecipitation); Transfection; CCK8; Colony Formation Assay; Cell Cycle Assay; Annexin V/PI Flow Cytometry; Western Blot; IHC (Immunohistochemistry); In Vivo Animal Model; Bioinformatics Analysis; Clinical Sample Validation |
| Clinical significance: |
circHIPK3 is increased in PTX-resistant tumor tissues and proposed as a therapeutic target for PTX-resistant breast cancer. |
| Description: |
circHIPK3 is up-regulated in paclitaxel-resistant breast cancer tissues and cells. Functionally, circHIPK3 promotes PTX resistance, while its knockdown sensitizes resistant cells and xenografts to PTX by sponging miR-1286 and thereby increasing HK2 expression, with associated suppression of glycolysis and malignant phenotypes upon circHIPK3 silencing. |
| Confidence score: |
0.8174 |