Schizandrin A inhibits cellular phenotypes of breast cancer cells by repressing miR‐155

• Published in: IUBMB life Vol. 72; no. 8; pp. 1640 - 1648
• Main Authors: Yan, Huiling, Guo, Meng
• Format: Journal Article
• Language: English
• Published: Hoboken, USA John Wiley & Sons, Inc 01-08-2020; Wiley Subscription Services, Inc
• Subjects: 1-Phosphatidylinositol 3-kinase; AKT protein; Annexin V; Apoptosis; Breast cancer; Cell migration; Cell proliferation; cellular phenotypes; Cholecystokinin; microRNA‐155; miRNA; Oxidation; Phenotypes; Propidium iodide; Schizandrin A; Western blotting; Wnt protein; microRNA-155; breast cancer; Schizandrin A; cellular phenotypes
• ISSN: 1521-6543; 1521-6551
• DOI: 10.1002/iub.2329

Aims
Schizandrin A (SchA) is a type of lignan with biological properties against oxidation, inflammation, and cancer. Here, we aimed to sustain the bioactive properties of SchA in proliferative and motional phenotypes of MDA‐MB‐231 cells and their molecular mechanism.
Methods
MDA‐MB‐231 cells were exposed to SchA. At 24 h after SchA treatment, the viability and proliferation were measured using CCK‐8 and BrdU incorporation methods, respectively. Propidium iodide/Annexin V‐FITC staining was carried out for detecting apoptotic cells. Migration and invasion were detected by 24‐Transwell assay. Proteins expression was evaluated by Western blotting. MDA‐MB‐231 cells were transfected with microRNA (miR)‐155 mimic, and miR‐155 was detected by qRT‐PCR.
Results
SchA weakens the viability of MDA‐MB‐231 cells in a dose‐relative way (0–40 μM). Furthermore, 30 μM SchA significantly suppresses proliferation, enhances apoptosis, and inhibits migration and invasion. SchA strikingly decreases miR‐155. Exogenous miR‐155 counteracts the inhibitory effects that SchA confers on proliferative and motional activities. Finally, SchA was observed to blunt PI3K/AKT and Wnt/β‐catenin while miR‐155 mimic reverses the effects.
Conclusion
Taken together, SchA downregulates miR‐155 and results in the suppression of proliferation and motility in breast cancer cells. Our findings proposed that SchA might be used as an underlying therapeutic agent.