Circular RNA circVEGFC accelerates high glucose-induced vascular endothelial cells apoptosis through miR-338-3p/HIF-1α/VEGFA axis.

More and more findings illustrate the critical roles of circular RNA (circRNA) in diabetes mellitus (DM) and its complications. A major pathological characteristic for DM is the apoptosis of endothelial cells (ECs) induced by high glucose (HG), however, the function of circRNA in the ECs' phenotypes is still elusive. Here, this study identified an up-regulated circRNA (circVEGFC) in the HG-induced human umbilical vein endothelial cells (HUVECs). Functionally, knockdown of circVEGFC alleviated the apoptosis and recovered the proliferation in HUVECs induced by HG administration. Mechanistically, circVEGFC functioned as the sponge of miR-338-3p, and miR-338-3p was found to target the 3'-Untranslated Regions (3'-UTR) of hypoxia inducible factor 1 alpha (HIF-1α). HIF-1α, a critical transcription factor in DM, could activate the transcription of vascular endothelial growth factor A (VEGFA) and promote its protein product. In conclusion, these findings reveal the promotion of circVEGFC/miR-338-3p/HIF-1α/VEGFA axis in the HG-induced ECs' apoptosis, providing a potential treatment strategy for ECs' damage in DM.

Long noncoding RNA MSC-AS1 promotes hepatocellular carcinoma oncogenesis via inducing the expression of phosphoglycerate kinase 1.

BACKGROUND AND OBJECTIVES: Increasing studies report that lncRNAs are dysregulated in hepatocellular carcinoma (HCC), which might function as significant diagnostic biomarkers of HCC. LncRNA MSC-AS1 has been newly discovered in several cancers. However, its biological effect in HCC remains to be clearly elucidated. The aim of our work was to test MSC-AS1 expression level and assess its function in HCC progression. METHODS: Expression levels of MSC-AS1 and PGK1 in HCC were tested by qRT-PCR in HCC cells including HUH-7, BEL-7404, SNU449, HepG2, QGY-7701, and human normal liver cells (HL-7702 cells). Association of MSC-AS1 expression with various clinicopathological features and patients' survival were analyzed by chi-squared test and Kaplan-Meier, respectively. The functions of MSC-AS1 in HCC cells were investigated using EdU assay, colony formation, flow cytometry, would healing assay, and Transwell matrigel invasion assays. The correlation between MSC-AS1 and PGK1 was confirmed using a RIP assay. Protein expression of PGK1 was evaluated using a western blot assay. RESULTS: MSC-AS1 was obviously upregulated in HCC tissues and HCC cells. Knockdown of MSC-AS1 repressed HepG2 and BEL-7404 cell proliferation, colony formation capacity, and triggered cell apoptosis. HepG2 and BEL-7404 cell cycle was blocked in G1 phase and cell migration/invasion was remarkably depressed. Downregulation of MSC-AS1 in HCC cells reduced PGK1 expression. In vivo data demonstrated that silence of MSC-AS1 suppressed HCC development via activating PGK1. CONCLUSIONS: Taken these together, we indicated that MSC-AS1 promoted HCC oncogenesis via inducing the expression of PGK1.

Dietary ginger as a traditional therapy for blood sugar control in patients with type 2 diabetes mellitus: A systematic review and meta-analysis.

BACKGROUND: Ancient medical practitioners used to encourage dietary supplements and herbal medicine for the treatment of type 2 diabetes mellitus (T2DM). Ginger (Zingiber officinale), is a nontoxic spice with negligible side effects, and is considered safe by the food and drug administration. In this analysis, we aimed to systematically compare fasting blood sugar (FBS) and glycated hemoglobin (HbA1c) at baseline versus at follow-up in T2DM patients who consumed and who did not consume ginger. METHODS: A literature search was carried out through MEDLINE, Embase, the Cochrane Central, and www.ClinicalTrials.gov for English-published trials comparing glucose parameters in T2DM patients who were assigned to ginger consumption versus a control group. All the participants were patients with T2DM who were either assigned to ginger therapy (1600- 4000 mg daily) or to a control group. FBS and HbA1c were assessed in the ginger and control groups, respectively, from baseline to follow-up to observe any significant change. Weight mean difference (WMD) with 95% confidence intervals (CI) was calculated to represent the analysis which was carried out by the RevMan 5.3 software. RESULTS: Eight randomized trials consisting of a total number of 454 participants with T2DM were included in this analysis. At first, FBS was compared in patients with T2DM from baseline prior to ginger consumption until follow-up after ginger consumption. The results showed no significant difference in FBS (WMD: 1.38, 95% CI: [-0.53-3.30]; P = .16). For the T2DM patients who did not consume ginger, no significant difference in FBS was observed (WMD: -0.27, 95% CI: [-5.09-4.54]; P = .91). However, a significantly improved HbA1c from baseline to follow-up was observed in those participants with ginger consumption (WMD: 0.46, 95% CI: [0.09-0.84]; P = .02) whereas in the control group, no significant difference in HbA1c was observed (WMD: -0.23, 95% CI: [-0.60-0.14]; P = .22). CONCLUSION: This analysis involving patients with T2DM showed no significant difference in FBS with ginger consumption. However, dietary ginger significantly improved HbA1c from baseline to follow-up showing that this natural medicine might have an impact on glucose control over a longer period of time in patients with T2DM.