Objective: To investigate the effects of miR-143-3p and MAPK7 on the proliferation, migration, and invasion of U2OS human osteosarcoma (OS) cells. Methods: The expression of miR-143-3p and MAPK7 in U2OS cells were detected by qRT-PCR, and the protein level of MAPK7 was measured by western blot assay. The targeting relationship between miR-143-3p and MAPK7 was predicted by TargetScan and verified by dual luciferase reporter assay. MTT and Transwell assays were used to detect cell viability, migrated cells and invaded cells of U2OS cells. Results: Compared with hFOB1.19 cells, the expression of miR-143-3p was down-regulated and MAPK7 was up-regulated in U2OS cells. Cell viability, migration and invasion ability significantly decreased induced by miR-143-3p overexpression or MAPK7 knockdown in U2OS cells. The results of dual luciferase reporter assay indicated that miR-143-3p interacted with MAPK7. Furthermore, overexpression of MAPK7 could reverse the inhibitory effects on cell proliferation, migration and invasion in U2OS cells induced by miR-143-3p mimics. Conclusion: miR-143-3p could inhibit proliferation, migration and invasion of U2OS cells by targeting MAPK7.

A versatile strategy is developed for the detection of tumor cells by combining aptamer-based specific cell recognition and EXPAR-based signal amplification.

Modern pharmacological studies revealed that Celastrol exhibits anti‑inflammation, anti‑bacteria, anti‑virus, anti‑fertility, insect‑resistance functions and has been used for the treatment of rheumatism, rheumatoid arthritis, blood diseases, skin diseases and agricultural insecticide. The present study aimed to investigate the effects of Celastrol on glucocorticoid‑induced osteoporosis (GIOP) and the underlying molecular mechanisms. The findings of the current study revealed that Celastrol reduced body weight, urine calcium/creatinine, tartrate‑resistant acid phosphatase 5b, C‑terminal telopeptide of type I collagen, and induced osteocalcin in GIOP rats. In addition, alkaline phosphatase, triiodothyronine receptor auxiliary protein and cathepsin K mRNA expression levels were effectively suppressed, and osteocalcin, bone morphogenetic protein 2, type I collagen and runt‑related transcription factor 2 mRNA expression levels were effectively induced in osteoporosis rats treated with Celastrol. Celastrol inhibited prostaglandin E2 and caspase‑3 protein expression levels, and induced phosphoinositol 3‑kinase (PI3K), phosphorylated‑protein kinase B (AKT) and glycogen synthase kinase‑3 phosphorylation, Wnt and β‑catenin protein expression in GIOP rats. The present study demonstrated that Celastrol may inhibit GIOP in rats via the PI3K/AKT and Wnt signaling pathways.