This study aimed to investigate the effects and regulatory mechanism of long non-coding RNA HEIH in the development of breast cancer. The expression of HEIH in breast tumor tissues and… Click to show full abstract
This study aimed to investigate the effects and regulatory mechanism of long non-coding RNA HEIH in the development of breast cancer. The expression of HEIH in breast tumor tissues and breast cancer cells was determined, followed by investigating the effects and regulatory mechanism of HEIH dysregulation on breast cancer cell viability, apoptosis, migration and invasion. The expression of HEIH was upregulated in breast cancer tissue samples and cell lines. Suppression of HEIH inhibited cell viability, promoted cell apoptosis, and decreased migration and invasion in MDA-MB-231 cells. Moreover, a negative relationship existed between HEIH and miR-200b, and HEIH regulated breast cancer development via regulating miR-200b. Pre-leukemia transcription factor 3 (PBX3) was verified as a functional target of miR-200b, and miR-200b regulated the malignant behaviors of breast cancer cells through targeting PBX3. Furthermore, suppression of HEIH inhibited the activation of Wnt/β-catenin pathway, which was remarkably reversed after suppression of HEIH and inhibition of miR-200b synchronously. Our results reveal that HEIH may contribute to breast cancer development via modulation of microRNA-200b/axis and inducing the activation of Wnt/β-catenin pathway. Further studies are still required to confirm our findings.
               
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