MicroRNA (miR)-92 expression is often aberrant in human cancers. However, its expression in gastric carcinoma and its relation to clinicopathological features and prognosis are unclear.Tissue microarrays were constructed from 180 patients with gastric cancer (GC), who were undergoing radical resection. MiR-92a expression was detected using miRNA-locked nucleic acid in situ hybridization, and its correlation with clinicopathological features and overall survival was analyzed. MiR-92a expression was decreased in 13.9 % (25/180) of GC, increased in 81.1 % (146/180), and unchanged in 5.0 % (9/180), compared with paracancerous normal tissue (P < 0.001). Univariate analysis showed that high miR-92a expression, tumor stage, tumor status, node status, and tumor size were significant negative prognostic predictors for overall survival in patients with GC (P < 0.001, P < 0.001, P = 0.008, P < 0.001, and P = 0.001, respectively). High miR-92a expression still remained a significant predictor of shorter survival in stage II (n = 56, P = 0.001) and stage III (n = 92, P = 0.009) GC. Multivariate regression analysis demonstrated that tumor status (hazard ratio [HR], 3.10; 95 % confidence interval [CI], 1.51-6.37; P = 0.002), stage (HR, 3.54; 95 % CI, 1.65-7.63; P = 0.000), lymph node metastasis (HR, 2.83; 95 % CI, 1.88-4.28; P = 0.000), high expression of miR-92a (HR, 2.94; 95 % CI, 2.01-4.31; P = 0.000), and tumor size (HR, 2.34; 95 % CI, 1.45-3.79; P = 0.002) predicted shorter OS.High expression of miR-92a compared with adjacent normal tissues was associated with shorter OS. MiR-92a may thus be useful for evaluating prognosis and may provide a novel treatment target in patients with GC.

The involvement of histone modifications in cartilage development, pathology and regeneration is becoming increasingly evident. Understanding the molecular mechanisms and consequences of histone modification enzymes in cartilage development, homeostasis and pathology provides fundamental and precise perspectives to interpret the biological behavior of chondrocytes during skeletal development and the pathogenesis of various cartilage related diseases. Candidate molecules or drugs that target histone modifying proteins have shown promising therapeutic potential in the treatment of cartilage lesions associated with joint degeneration and other chondropathies. In this review, we summarized the advances in the understanding of histone modifications in the regulation of chondrocyte fate, cartilage development and pathology, particularly the molecular writers, erasers and readers involved. In addition, we have highlighted recent studies on the use of small molecules and drugs to manipulate histone signals to regulate chondrocyte functions or treat cartilage lesions, in particular osteoarthritis (OA), and discussed their potential therapeutic benefits and limitations in preventing articular cartilage degeneration or promoting its repair or regeneration.