Breast cancer is the most common malignancy in women and is a molecularly heterogeneous disease. Signal transducer and activator of transcription 3 (Stat3) is overexpressed and hyperactivated in a variety of human tumours, including breast cancer, thus representing a promising target for breast cancer treatment. In the present study, we evaluated the activities of a novel Stat3 inhibitor named Statmp-151 in the human breast cancer cell lines MCF-7 and MDA-MB-231 and the murine mammary carcinoma cell line 4T1. The in vitro results showed that Statmp-151 inhibited the proliferation of breast cancer cell lines in a dose- and time-dependent manner and suppressed the phosphorylation of Stat3 in a dose-dependent manner. Flow cytometry (FCM) assays revealed that Statmp-151 affected mitochondrial membrane potential and reactive oxygen species (ROS) production. Furthermore, Statmp-151 inhibited cell migration, as shown by analysis of the matrix metalloproteinases MMP2 and MMP9. Finally, in a 4T1 tumour-bearing mouse model, intraperitoneal injection of 30 mg/kg/day Statmp-151 significantly suppressed the growth of tumours without obvious toxicity. These results indicated that Statmp-151 might be a potential candidate for the treatment of breast cancer.

We aimed to investigate the function and its possible mechanisms of long noncoding RNA (lncRNA) in acute myocardial infarction (AMI) model. Patients with AMI and normal volunteers were selected from our hospital. Sprague-Dawley rats were induced into in vivo model of AMI. H9c2 cells were treated with H 2 O 2 to generate injury model. A significantly lower serum gene expression of lncRNA CASC2 was detected. In rat models of AMI, lncRNA CASC2 gene expressions in heart tissue of mice with AMI were decreased. In in vitro model, downregulation of lncRNA CASC2 increased reactive oxygen species (ROS)-induced oxidative stress; lncRNA CASC2 induced NADPH oxidase (NOX-2) expression and suppressed miR-18a expression; MiR-18a promoted ROS-induced oxidative stress; downregulation of miR-18a decreased ROS-induced oxidative stress. The inhibition of miR-18a reversed the effects of CASC2 downregulation on ROS-induced oxidative stress in in vitro model of AMI. The activation of miR-18a reversed the effects of CASC2 on ROS-induced oxidative stress in in vitro model of AMI. These data for the first time suggest that lncRNA CASC2 have better protective effects on AMI, which could reduce oxidative stress through their carried miR-18a and subsequently downregulating the SIRT2/ROS pathway.

Objective: To delve into the correlation between miR-92b expression in peripheral plasma and hypertension, heart disease and cerebral hemorrhage. Methods: We enrolled 204 patients hospitalized in our institution from March 2016 to May 2017, including patients with hypertension (group B), hypertensive left ventricular hypertrophy (HTN-LVH) (group C), HTN-LVH complicated heart failure (group D), with 68 cases each group, and recruited another 60 healthy volunteers as control group (group A). Our team compared miR-92b level in peripheral plasma, and ultrasound indexes among the four groups and inquired into their correlation. The patients were followed up to assay miR-92b level in the peripheral plasma, cerebral edema volume and cerebral hematoma volume before and after treatment. Results: (1) In contrast to group B, the LVDs and LVMI in group C, D waxed, whereas LVEF and E/A waned (P<0.05). In contrast to group C, group D owned increased LVDs and LVMI, and decreased LVEF (all P<0.05). (2) In contrast to group A, miR-92b expression decreased in groups B, C and D, among which group D were the lowest and group B were the highest (all P<0.05). (3) miR-92b held negative relationship with SBP, DBP, LVDd and LVMI (all P<0.001), and had positive link with LVEF (r=0.649, P<0.001). (4) In contrast to before treatment, miR-92b expression in plasma was up-regulated after treatment (P<0.05). miR-92b level in plasma after treatment possessed negative association with brain edema volume and hematoma volume (P<0.001), and no correlation with the edema/hematoma ratio. Conclusion: miR-92b expression in peripheral plasma of patients with hypertension, myocardial hypertrophy and cerebral hemorrhage is down-regulated. miR-92b probably harbors a defensive impact and participates in the pathophysiological process of hypertension, heart disease and cerebral hemorrhage.