MiR-548b-3p inhibits proliferation and migration of breast cancer cells by targeting MDM2.

OBJECTIVE: The aim of this study was to explore the expression and biological functions of micro ribonucleic acid (miR)-548b-3p in breast cancer (BC), and to investigate its potential molecular mechanism. PATIENTS AND METHODS: The expression level of miR-548b-3p in BC tissues and cells was detected by quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR). Subsequently, the impacts of miR-548b-3p on the proliferation, apoptosis, and cycle, as well as migration and invasion of BC cells, were explored using colony formation assay and 5-ethynyl-2'-deoxyuridine (EdU) staining, flow cytometry, and transwell assay, respectively. The possible downstream target genes of miR-548b-3p were predicted via bioinformatics and verified through qRT-PCR and Western blotting. Furthermore, Dual-Luciferase reporter gene assay was employed to confirm whether miR-548b-3p could directly bind to murine double minute 2 (MDM2). RESULTS: QRT-PCR results showed that miR-548b-3p expression was significantly downregulated in 37 out of 43 BC tissues. Subsequent in-vitro experiments indicated that the overexpression of miR-548b-3p significantly inhibited the proliferation and metastasis, whereas promoted the apoptosis of BC cells. Bioinformatics predicted that MDM2 was the downstream target gene of miR-548b-3p. After overexpression of miR-548b-3p, qRT-PCR, and Western blotting results revealed that the expression of MDM2 was remarkably downregulated. Dual-Luciferase reporter gene assay further confirmed that miR-548b-3p could directly bind to MDM2. CONCLUSIONS: MiR-548b-3p expression was significantly downregulated in BC. In addition, lowly expressed miR-548b-3p repressed the proliferation and metastasis of BC cells through targeted regulation of MDM2.

Effects of Vitamin B12 on postoperative cognitive dysfunction induced by isoflurane anesthesia in rats.

OBJECTIVE: Postoperative cognitive dysfunction is a clinical syndrome associated with cognitive decline in patients after anesthesia. This study aimed to investigate the effect of VB12 (Vitamin B12), a kind of necessary micronutrients promoting the growth and development of the nervous system, on cognitive dysfunction induced by isoflurane anesthesia. MATERIALS AND METHODS: Eighteen-month-old rats were exposed to or were not exposed to 1.4% isoflurane for 2 h. Two hours before isoflurane exposure, rats in groups with VB12 were injected intramuscularly with VB12 at 10 or 20 µg. Two weeks later, rats were subjected to Barnes maze and Morris water maze. RESULTS: Rats exposed to isoflurane had significant impairments in long-term spatial memory assessed by Barnes maze. There was no statistical significance in the percentage of swimming time and path length in the Morris water maze tests among five groups, suggesting that isoflurane may not impair the recall of learned information in rats. Isoflurane increased the expression of interleukin 1ß (IL-1ß) and activated caspase 3 in the hippocampus, but not cortex of the rats. The increase of IL-1ß and activated caspase 3 was attenuated by VB12. However, isoflurane did not change the amount of tumor necrosis factor-α (TNF-α) and ß-amyloid peptide in the hippocampus and cerebral cortex. CONCLUSIONS: VB12 can attenuate cognitive dysfunction induced by isoflurane anesthesia. At the same time, IL-1ß may play an important role in this isoflurane effect.