We planned to dig the carcinostasis activity of physcion 8-O-b-glucopyranoside (PG) in ovarian cancer cells and explored whether long non-coding RNA NORAD was the potential cause of the carcinostasis impact of PG. The impacts of PG on the tumour cell behaviours (including cell viability, apoptosis, migration and invasion) of SKOV3 cells were grabbed. The levels of NORAD in cancer tissues and cell lines were determined; afterwards, the impacts of abnormal expression of NORAD on the tumour cell behaviours of SKOV3 cells were assessed. Moreover, we explored whether NORAD modulated the level of STAT3 by competitively sponging miR-608, thus mediating the antineoplastic effects of PG on ovarian cancer cells. PG suppressed cell viability, enhanced apoptosis and lessened migration and invasion of SKOV3 cells. NORAD was upregulated in ovarian cancer tissues and cells. Silencing of NORAD lessened cell viability, migration and invasion, but induced apoptosis of SKOV3 cells, whereas overexpression of NORAD had opposite effects. Moreover, PG decreased the expression of NORAD. Overexpression of NORAD reversed the effects of PG treatment on the cell biological performances of SKOV3 cells, which were further reversed after overexpression of miR-608 simultaneously. Furthermore, STAT3 was tested as a target gene of miR-608, and the impact of NORAD in PG-treated SKOV3 cells were through the miR-608-mediated STAT3. Our findings reveal that NORAD/miR-608/STAT3 axis is pivotal in mediating the antineoplastic impacts of PG on ovarian cancer cells, which may offer a novel explanation in the therapy of ovarian cancer.

Background: miRNAs participate in the development and progression of diabetic retinopathy (DR). High expression of NF-κB signaling pathway boosts the progression of retinopathy in diabetes rats. We found a site where miR-874 bound to the NF-κB p65 by a bioinformatics website. Therefore, we speculated that miR-874 might improve retinopathy in diabetic rats by inhibiting the NF-κB signaling pathway. Methods: Ten healthy rats were taken as the control group. Sixty streptozotocin (60 mg/kg)-induced diabetes model rats were randomly divided into the model group (injection of normal saline), NC (negative control) agomir group (injection of NC mimic), miR-874 agomir group (injection of miR-874 mimic), miR-874 anti-agomir group (injection of miR-874 inhibitor), EVP4593 group (injection of NF-κB signaling pathway antagonist EVP4593), and miR-874 anti-agomir + EVP4593 group (injection of miR-874 inhibitor and EVP4593). All injection was via caudal vein. Results: miR-874 could target the degradation of p65. Compared with the control group, model rats had reduced miR-874 expression, increased VEGF and Ang2 protein expressions, lowered end-diastolic velocity and peak systolic velocity of central retinal artery (CRA) and blood velocity of central retinal vein and CRA, heightened plasma viscosity, blood viscosity and erythrocyte sedimentation rate at all shear rates, decreased capillary pericytes, increased vascular endothelial cells, and ascended p65 expression in the retina (all P < 0.05). It showed that pathological changes appeared in the retina of diabetes rats. These indexes would be improved in diabetes rats injected with miR-874 mimic or EVP4593, but deteriorated in those injected with miR-874 inhibitor (all P < 0.05). EVP4593 could alleviate the aggravation of retinopathy that was caused by miR-874 inhibition in diabetes rats. Conclusions: miR-874 mediates the NF-κB signaling pathway by targeting the degradation of p65 to further improve the retina of diabetes rats, showing the improvement effect of miR-874 on diabetic retinopathy in rats.

Background: This study aimed to explore the improvement effect of miR-874 on retinopathy in diabetic rats by NF-κB signaling pathway. Methods: Ten healthy Sprague-Dawley rats were taken as the control group. Sixty streptozotocin (60 mg/kg)-induced diabetes model rats were randomly divided into model group (without any treatmentinjection of normal saline), negative control (NC) agomir group (injection of overexpressed NC vector), miR-874 agomir group (injection of miR-874 mimic), miR-874 anti-agomir group (injection of miR-874 inhibitor), EVP4593 group (injection of NF-κB signaling pathway antagonist EVP4593), and miR-874 anti-agomir + EVP4593 group (injection of miR-874 inhibitor and EVP4593). All injection was via caudal vein. Results: miR-874 could target the degradation of p65. Compared with control group, there were significantly reduced miR-874 expression, increased VEGF and Ang2 protein expressions, lowered end-diastolic velocity and peak systolic velocity of central retinal artery (CRA), and blood velocity of central retinal vein and CRA, heightened plasma viscosity, blood viscosity and erythrocyte sedimentation rate at all shear rates, decreased capillary pericytes, increased vascular endothelial cells, and ascended p65 expression in the retina of rats in model group (all P < 0.05). It showed that pathological changes were happened on the retina of diabetes rats. These indexes showed the same results after miR-874 was inhibited (all P < 0.05). However, these indexes showed the opposite results in miR-874 agomir group and EVP4593 group compared with model group (all P < 0.05). EVP4593 could alleviate the aggravation of retinopathy caused by the inhibition of miR-874 in diabetes rats. Conclusions: miR-874 mediates NF-κB signaling pathway by targeting the degradation of p65 to further improve the retina of diabetes rats, showing the improvement effect of miR-874 on diabetic retinopathy in rats.