SNHG17/miR-384/ELF1 axis promotes cell growth by transcriptional regulation of CTNNB1 to activate Wnt/ß-catenin pathway in oral squamous cell carcinoma.

Increasing evidence proved the abnormal expression of long non-coding RNAs (lncRNAs) in various human malignancies, including oral squamous cell carcinoma (OSCC). Nevertheless, limited explorations concern the role of lncRNA small nucleolar RNA host gene 17 (SNHG17) in OSCC. Herein, SNHG17 was disclosed to be remarkably upregulated in OSCC cell lines and promoted OSCC cell growth. Further mechanistic studies, including DNA/RNA pull down, RIP, ChIP, and luciferase reporter gene assays, were conducted. It was confirmed that Wnt/ß-catenin signaling pathway was involved in the SNHG17-mediated OSCC cell growth. Moreover, E74 like ETS transcription factor 1 (ELF1) was identified as the transcription activator of CTNNB1 (ß-catenin mRNA) in OSCC. Inspired by competing for endogenous RNAs (ceRNAs) network, we were pleasantly surprised to find that SNHG17 and ELF1 functioned as ceRNAs in OSCC via competitively binding to microRNA-384 (miR-384). By using rescue assays, we revealed that SNHG17 facilitated OSCC cell growth through modulating miR-384/ELF1 axis. Importantly, we certified that ELF1 was indispensable for SNHG17-affected OSCC progression. Collectively, it can be concluded that SNHG17/miR-384/ELF1 axis contributed to OSCC cell growth via promoting CTNNB1 expression, thus activating Wnt/ß-catenin signaling pathway.

Anticancer effects and possible mechanisms of lycopene intervention on N-methylbenzylnitrosamine induced esophageal cancer in F344 rats based on PPARγ1.

Lycopene, a natural carotenoid, has potential chemopreventive effects in many cancers. This study aimed to examine the effects of lycopene on regulating the inflammation and apoptosis of N-nitrosomethylbenzylamine(NMBzA) induced esophageal cancer in F344 rats. After the rats were fed normal diets containing different concentrations of lycopene for 25 weeks (10, 25, 50 mg/kg·d of lycopene, respectively), the incidence of tumors in the rats treated with lycopene was significantly lower than that in the simple exposed group (P < 0.05). The antioxidant activity of lycopene was exerted by measuring the levels of GSH-PX, SOD and MDA activity by oxidative stress kits. Furthermore, through western blotting analysis lycopene intervention was found to have significantly improved apoptosis cytokines by increasing the protein expression levels of PPARγ and caspase-3, and also significantly reduced inflammatory cytokines by decreasing the protein expression of NF-κB and COX-2 in the esophagus tissue, especially in the 25 mg/kg of lycopene intervention group (all P < 0.05). These results demonstrated that appropriate dose of lycopene intervention could inhibit the carcinogenesis of esophageal in F344 rats through the possible mechanisms of anti-inflammatory and pro-apoptosis.

Circulating irisin levels of prenatal and postnatal patients with gestational diabetes mellitus: A systematic review and meta-analysis.

AIMS: At present, there are few studies on the relationship between circulating irisin levels and gestational diabetes mellitus (GDM), and the results are inconsistent. Therefore, this study conducts a systematic review and meta-analysis to comprehensively discuss the role of irisin in the occurrence and development of GDM. METHODS: We searched the articles on the relationship between GDM and circulating irisin levels up to September 2019, using the CNKI, WANFANG-DATA, PubMed and the Web of Science databases. RESULTS: Twenty two articles including 3563 participants were selected in the meta-analysis. Meta-analysis found the blood irisin levels for GDM group were significantly lower than that for control group during pregnancy(SMD = -0.88, 95%CI: -1.34, -0.42, P < 0.001). However, there was no significant difference of irisin levels in the postpartum blood and cord blood between the two groups (SMD = -1.44, 95 %CI: -3.79, 0.92, P = 0.23; SMD = -0.17, 95 %CI: -0.59, 0.25, P = 0.42, respectively). CONCLUSIONS: Compared with the control group, irisin levels in the GDM group during pregnancy are lower. However, it is no significant difference of irisin levels in the postpartum blood and cord blood. Irisin may play an important role in the occurrence and development of GDM, which needs further research to demonstrate.

Dietary natural astaxanthin at an early stage inhibits N-nitrosomethylbenzylamine-induced esophageal cancer oxidative stress and inflammation via downregulation of NFκB and COX2 in F344 rats.

Purpose: Esophageal cancer is a common malignant tumor that develops rapidly and has a poor prognosis clinically. Astaxanthin (AST) is a carotenoid pigment with strong antioxidant, anti-inflammation, and antitumor activities. However, little is known about the effects of astaxanthin in esophageal cancer. The present study aimed to investigate the protective effects and related mechanisms of natural astaxanthin against N-nitrosomethylbenzylamine (NMBA)-induced esophageal cancer in rats. Methods: F344 rats were induced subcutaneously with NMBA dissolved in dimethyl sulfoxide (0.35 mg/kg body weight three times per week for 5 weeks). Rats were fed normal diets with or without 25 mg/kg/day AST at different stages. At different time points, levels of oxidative stress factors in serum and esophagus tissue were analyzed. Western blotting was performed to observe the expression of NFκB and COX2 in esophagus tissue. Results: AST clearly reduced the incidence of visible tumors in esophageal cancer during the early-stage intervention group. Furthermore, when compared with the simple exposed group, AST significantly increased levels of GPx and SOD activity, decreased the activity level of malondialdehyde (all P<0.05). Early-stage and whole-stage intervention groups effectively attenuated expression levels of NFκB and COX2 proteins compared with the simple exposed group (all P<0.05). Conclusion: Natural AST significantly suppressed the occurrence of esophageal cancer by increasing antioxidant capacity and anti-inflammation capacity by inhibiting expression levels of NFκB and COX2 proteins.

Association between Dietary Vitamin E Intake and Esophageal Cancer Risk: An Updated Meta-Analysis.

Epidemiological studies have provided ambiguous evidence on the association between vitamin E and esophageal cancer risk. To resolve this controversy, we performed this meta-analysis. The literature was searched by using Excerpta Medica Database (EMBASE), PubMed, the Web of Science, and the Cochrane Library from the inception to April 2018. A random effect model was utilized to calculate the odds ratio (OR) with the 95% confidence interval (95% CI). Twelve articles reporting 14 studies involving 3013 cases and 11,384 non-cases were included. By comparing the highest category with the lowest category of dietary vitamin E intake, we found that dietary vitamin E intake was inversely related to esophageal cancer risk (OR = 0.47, 95% CI: 0.36⁻0.60). Subgroup analysis revealed that dietary vitamin E intake had a significantly negative association with both the esophageal squamous cell carcinoma risk (OR = 0.29, 95% CI: 0.18⁻0.44) and the esophageal adenocarcinoma risk (OR = 0.66, 95% CI: 0.49⁻0.88). No study significantly affected the findings in the sensitivity analysis. Publication bias was discovered, however, the OR (95% CI) remained unchanged after the trim-and-fill analysis. This meta-analysis showed that the higher dietary vitamin E intake is associated with a lower esophageal cancer risk. However, the association still needs to be upheld by more large-scaled randomized controlled trials and prospective studies.