Effects of NEAT1 levels on cardiovascular events and prognosis in diabetic nephropathy patients undergoing peritoneal dialysis.

The purpose of this study was to provide observational indicators for clinically predicting cardiovascular events in patients with diabetic nephropathy (DN) undergoing peritoneal dialysis by determining the effects of nuclear enriched abundant transcript 1 (NEAT1) levels on the cardiovascular events and prognosis in DN patients receiving continuous ambulatory peritoneal dialysis (CAPD). A retrospective analysis was conducted on the data of 80 DN patients undergoing CAPD. Patients were assigned to NEAT1 high expression group and NEAT1 low expression group. NEAT1 had a substantially increased expression in the serum of DN patients, and it could serve as a potential biomarker for predicting the development of DN. Patients with highly expressed NEAT1 had an higher level of high-sensitivity C-reactive protein (hs-CRP), larger cardiac structural parameters left ventricular end-diastolic diameter (LVED), left ventricular end-systolic diameter (LVESD), interventricular septal diameter (IVSD) and left ventricular posterior wall diameter (LVPWD), but a notably lower cardiac function evaluation indicator left ventricular ejection fraction (LVEF) than those with lowly expressed NEAT1. The coefficient (r) of correlation between NEAT1 and hs-CRP level was 0.3585 (P=0.0011). The incidence rates of acute myocardial infarction, congestive heart failure and angina in NEAT1 high expression group were higher than those in NEAT1 low expression group. Patients with NEAT1 high expression exhibited a higher mortality rate than NEAT1 low expression group. With the increase in NEAT1 levels, the level of hs-CRP rose in DN patients undergoing CAPD. A higher expression level of NEAT1 indicates poorer cardiac function, higher incidence rates of cardiovascular adverse events and a poorer prognosis in diabetics undergoing CAPD.

LINC01311 exerts an inhibitory effect in thyroid cancer progression by targeting the miR-146b-5p/IMPA2 axis.

BACKGROUND: A growing body of research suggests that long non-coding RNA (lncRNA) play an important role during the tumorigenesis and progression of cancers, including thyroid cancer (TC). Herein, we intended to uncover the role and mechanisms of LINC01311 in TC. METHODS: The relative LINC01311, miR-146b-5p, and IMPA2 expressions were quantified by subjecting TC cells and tissues to western blotting and RT-qPCR. CCK-8 and scratch-wound healing assays were carried out for the evaluation of the proliferation and migration of TC cells. The apoptosis was evaluated by flow cytometry assay and western blotting of Bax and Bcl-2 proteins. Xenograft tumor model was also used to study how LINC01311 functions during TC cell growth. Luciferase reporter and RNA immunoprecipitation (RIP) assays were performed to ascertain miR-146b-5p's interactions with LINC01311 and IMPA2 3'UTR. RESULTS: The TC cells and tissues exhibited a downregulation of LINC01311 and IMPA2 and an upregulation of miR-146b-5p. LINC01311 overexpression retarded TC cell growth in vitro as well as in vivo. The luciferase reporter and RIP assays verified that miR-146b-5p recognizes LINC01311 and IMPA2 3'UTR by base pairing. LINC01311 overexpression could counteract the oncogenic effect of miR-146b-5p in vitro. Moreover, IMPA2 upregulation could offset the tumor-promoting effect of miR-146b-5p. CONCLUSION: LINC01311-mediated inhibition of TC cell growth was achieved by targeting the miR-146b-5p/IMPA2 axis. These findings support that targeting the LINC01311/miR-146b-5p/IMPA2 axis may be a promising approach against TC progression.

Propofol induces hepatocellular carcinoma cell apoptosis via regulating miR-105/JAK2/STAT3 axis.

BACKGROUND: Hepatocellular carcinoma (HCC) is a type of malignancy with high mortality. It has been reported Propofol could modulate the tumorigenesis of liver cancer; however, the mechanism by which Propofol regulates the development of HCC is still not clear. METHODS: CCK8 assay was applied to test the cell viability. Flow cytometry and TUNEL staining were applied to detect the cell apoptosis. Meanwhile, dual luciferase reporter assay was performed to investigate the association between miR-105 and JAK2. In addition, RNA and protein levels were investigated by qRT-PCR and western blot, respectively. RESULTS: Propofol significantly suppressed the proliferation of HCC cells via inducing the apoptosis. Consistently, miR-105 upregulation inhibited the proliferation of HCC cells, while downregulation of miR-105 reversed Propofol-induced HCC cell apoptosis. Meanwhile, JAK2 was found to be the direct target of miR-105. Furthermore, Propofol could inactivate JAK2/STAT3 signaling via upregulation of miR-105. CONCLUSION: Propofol significantly attenuated HCC tumorigenesis via mediation of miR-105/JAK2/STAT3 axis. Thereby, Propofol might act as a new agent for the treatment of HCC.