Many studies have shown that microRNA regulates the development and treatment of osteosarcoma (OS). In many human cancer studies, the expression of microRNA-202 has been shown to be abnormal. The aim of the study was to examine the role of miR-202-5p in the occurrence and formation of OS. miR-202-5p and Rho-associated coiled-coil containing protein kinase 1 (ROCK1) levels were assessed using RT-qPCR in OS tissues and cell lines. The cell migrating and invasive abilities were detected by the Transwell assay in OS. Moreover, the relationship between miR-202-5p and ROCK1 was verified via luciferase reporter assay. The protein level of ROCK1 was identified by western blot analysis. Downregulation of miR-202-5p was identified in OS tissues and cell lines. In addition, the miR-202-5p overexpression had inhibitory action for cell migration and invasion in OS. Moreover, miR-202-5p directly targeted ROCK1 and negatively regulated its expression. Upregulation of ROCK1 had a carcinogenic effect in OS. Furthermore, the upregulation of ROCK1 restored the suppressive effect of miR-202-5p. miR-202-5p, in turn, weakened the abilities of cell migration and invasion in OS by inhibiting ROCK1 expression. As a result, miR-202-5p may be developed as a potential pathway in the reatment of OS.

Abstract. Acute coronary syndrome (ACS) typically occurs when coronary artery disease results in the obstruction of the coronary arteries. Tenascin-C (TNC) and OX40 ligand (OX40L) were shown to be involved in the pathogenesis of atherosclerosis. In this study, 50 healthy controls and 170 patients, including 50 patients with stable angina (SA), 70 with unstable angina and 50 with acute myocardial infarction, were evaluated to assess serum TNC and plasma OX40L levels. The serum TNC levels were measured by a quantitative automated particle-enhanced immunonephelometric assay. ELISA was used to determine the expression levels of OX40L. All the coronary stenoses with a ≥30% diameter reduction were assessed by angiographic coronary stenosis morphology. The patients with ACS exhibited a significant increase in TNC expression levels (39.39±19.80 ng/ml) compared to the levels in the control and SA groups (28.65±12.32 ng̸ml, P<0.01 and 31.22±18.92 ng/ml, P<0.05, respectively). The levels of OX40L were also found to be higher in patients with ACS (38.59±15.76 ng̸ml) compared to those in the control and SA groups (19.42±11.19 ng̸ml, P<0.001 and 21.52±10.30 ng/ml, P<0.001, respectively). The TNC and OX40L levels were positively correlated with each other (r 1 =0.68; P<0.001) and with fibrinogen levels (r 3 =0.76 and r 4 =0.45, respectively; P<0.001). A positive correlation was also observed between the expression of TNC and OX40L and complex coronary stenosis (r 5 =0.69 and r 6 =0.55, respectively; P<0.001). We concluded that TNC and OX40L may act synergistically in coronary plaque formation and may be also be involved in the pathogenesis of coronary lesions. Patients with ACS exhibited increased TNC and OX40L expression levels, which may have created a prothrombotic milieu, aggravating the development of atherosclerosis and the instability of atherosclerotic plaques. Therefore, the expression of TNC and OX40L may be a valuable marker for predicting the severity of ACS.

No abstract