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MicroRNA (miR)-22 has previously been reported to be frequently downregulated in certain types of cancer. The present study examined the expression and effects of miR-22 in renal cell carcinoma (RCC). The results indicated that miR‑22 was downregulated in tumor tissue from patients with RCC. In addition, lower miR‑22 expression levels were associated with histological grade, tumor stage and lymph node metas-tasis. Following transfection of RCC cells with miR‑22, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, cell migration, cell invasion and luciferase assays, and western blotting were conducted. The results demonstrated that miR‑22 was able to inhibit cell proliferation, migration and invasion in 786‑O and A498 cells. Furthermore, the results indicated that miR‑22 may directly target phosphatase and tensin homolog (PTEN) in RCC. In conclusion, the present study suggested that the miR-22/PTEN axis may be considered a novel therapeutic target in RCC. These findings may be beneficial for the development of an effective therapy against RCC.
This study was carried out in order to investigate bone dysfunction and the involvement of bradykinin receptors and the Eph/Ephrin signaling pathway in osteoblasts and in mice with diabetes-related osteoporosis in response to exposure to high glucose. Osteogenic transdifferentiation was inhibited when the osteoblasts were exposed to high glucose, and the expression levels of bone formation-related genes [Runx2 and alkaline phosphatase (ALP)] were decreased, while those of bone resorption-related genes [matrix metalloproteinase (MMP)9 and carbonic anhydrase II (CAII)] were increased. Moreover, the mRNA and protein expression levels of bradykinin receptor B1 (BK1R)/bradykinin receptor B2 (BK2R) and EphB2/EphrinB2 were significantly decreased in the osteoblasts following exposure to high glucose. Intriguingly, the interaction between BK2R and EphB2/EphrinB2 was confirmed, and BK2R loss-of-function significantly decreased the mRNA and protein expression levels of EphB2/EphrinB4. In vivo, hyperglycemia induced the disequilibrium of calcium homeostasis through the inhibition of bone formation and the acceleration of bone resorption, which was manifested by the reduction of trabecular bone mass of the primary and secondary spongiosa, as well as by the increase in the number of mature osteoclasts throughout the proximal tibial metaphysis in mice with diabetes-related osteoporosis. Furthermore, the mRNA and protein expression levels of BK1R/BK2R and EphB2/EphrinB2 in the tibias of the mice with diabetes-related osteoporosis were significantly decreased. These results demonstrate that bradykinin receptors and the EphB4/EphrinB2 pathway mediate the development of complications in mice with diabetes-related osteoporosis and suggest that the inactivation of bradykinin receptors and the EphB4/EphrinB2 pathway enhance the severity of complications in mice with diabetes-related osteoporosis.