AI Article Synopsis
- The study focused on understanding the role of LRP8 in breast cancer, finding it is highly expressed in cancer tissues and linked to poor patient outcomes.
- LRP8 levels were inversely related to miR-1262, which suppresses LRP8 expression and enhances tumor behavior in breast cancer cells.
- Reducing LRP8 or increasing miR-1262 decreased aggressive traits of breast cancer cells, suggesting that LRP8 promotes breast cancer progression regulated by miR-1262.
Article Abstract
This research was designed to detect the function of low-density lipoprotein receptor (LDLR)-related protein 8 (LRP8) in breast cancer (BC). Our results revealed that LRP8 was highly expressed in BC tissues and cell lines compared with human normal breast tissues. The poor prognosis of patients with BC was associated with the up-regulation of LRP8 while inversely connected with overexpression of miR-1262. Functionally, LRP8 depletion in BC cells impaired the proliferative, clonogenic, invasive, and migratory capabilities, which was consistent with the effects of upregulated miR-1262. Bioinformatics prediction and luciferase reporter assay confirmed that miR-1262 was an upstream factor for LRP8 and negatively regulated the expression of LRP8. Further experiments illustrated that the co-transfection of miR-1262 antamir and si-LRP8 could significantly suppress the promoting impacts caused by the transfection of miR-1262 antamir alone. These findings highlighted that LRP8 accelerated the BC development by contributing cellular aggressiveness, which was modulated by miR-1262.
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| http://dx.doi.org/10.1080/13813455.2020.1716019 | DOI Listing |
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