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Simple Summary: In this study, we investigated the effects of palmitic acid (PA) on multiple human gastric cancer cell lines and combined them with the results from clinical gastric cancer and paracancerous tissue samples. Our findings demonstrated that PA exerted anti-gastric cancer effects by regulating key molecules in the signal transduction and activation of a transcription 3 (STAT3) protein inhibitor of the activated STAT 3 (PIAS3) signaling pathway. Our results serve as a foundation for further research on the correlation between the anti-gastric cancer activity of PA and the STAT3-PIAS3 signaling pathway. Our results also represent a critical step toward understanding gastric cancer prevention and prognosis and promoting PA supplementation as a gastric cancer treatment. Lipidomic analyses have suggested that palmitic acid (PA) is linked to gastric cancer. However, its effects and action mechanisms remain unclear. Therefore, we evaluated the effects of PA on cell proliferation, invasion, and apoptosis in human gastric cancer, as well as the role of p-STAT3 in mediating its effects. The results of the MTT and colony formation assays revealed that PA blocked gastric cancer cell proliferation in a concentration-dependent manner. The EdU-DNA assay indicated that 50 μM of PA could block gastric cell proliferation by 30.6–80.0%. The Transwell assay also confirmed the concentration dependence of PA-induced inhibitory effect on cell invasion. The flow cytometry analysis indicated that PA treatment for 18 h could induce gastric cancer cell apoptosis. The immunohistochemical staining revealed that p-STAT3 levels were higher in the gastric cancer tissues than in the control tissues. We demonstrated that PA treatment for 12 h decreased the expressions of p-STAT3, p-JAK2, N-cadherin, and vimentin, and inhibited the nuclear expression of p-STAT3 in gastric cancer cells. Finally, PA treatment (50 mg/kg) decreased gastric cancer growth (54.3%) in the xenograft models. Collectively, these findings demonstrate that PA inhibits cell proliferation and invasion and induces human gastric cancer cell apoptosis. [ABSTRACT FROM AUTHOR]

Recently, long noncoding RNAs (lncRNAs) are attracting wide attention in the field of cancer research because of its important role in cancer diagnosis and prognosis. But studies on the biological effects and relevant mechanisms of lncRNAs in non‐small cell lung cancer (NSCLC) remain few and need to be enriched. Our study discussed the expression and biological effects of LncRNA NR2F2‐AS1, and further explored its possible molecular mechanisms. As a result, elevated expression of NR2F2‐AS1 was detected in NSCLC tissues and cells and was remarkably associated with the tumor, node, metastasis (TNM) stage and the status of lymphatic metastasis of patients. Down‐regulated NR2F2‐AS1 contributed to the promotion of cell apoptosis and the inhibition of cell proliferation and invasion in A549 and SPC‐A‐1 cells in vivo and vitro. Through bioinformatics analysis, NR2F2‐AS1 functions as a ceRNA directly binding to miR‐320b, BMI1 was a direct target of miR‐320b. Combined with the following cellular experiments, the data showed that NR2F2‐AS1 may influence the NSCLC cell proliferation, invasion and apoptosis through regulating miR‐320b targeting BMI1. [ABSTRACT FROM AUTHOR]

Aging may be a risk factor for type 2 diabetes in the elderly. Dietary intervention can affect glucose tolerance in adults, which may be due to body composition and islet cell autophagy. The aim of this study was to determine the effects of various dietary interventions on islet cell autophagy. Pancreatic tissue and blood samples were collected from Sprague Dawley rats (14–16 months old, n = 15 for each group) that received a normal diet (ND), a high-fat diet (HFD), or a calorie-restricted diet (CRD). The body weight (BW), visceral fat, serum lipid levels, fasting serum glucose, insulin levels, and β/α cell area were determined in 14-16-(0-w), 16-18-(8-w), and 18-20(16-w)-month-old rats. Pancreatic islet autophagy (LC3B and LAMP2), AP (Acid Phosphatase) and apoptosis (apoptosis index, AI (TUNEL assay) and cleaved caspase-3) were detected using immunohistochemistry, ELISA and western blot. At 16 weeks, the expressions of LC3B, LAMP2 and AP markedly increased in both the HFD (P<0.01) and CRD (P<0.05) groups; however, an increase in the AI (P<0.05), cleaved caspase-3 and Beclin1 expression and a decrease in the expressions of BCL2 and BCLXL (P<0.05) were observed in only the HFD group. FFA, triglyceride levels, HOMA-IR, insulin levels and glucagon levels were significantly increased in the HFD group but decreased in the CRD group at 16 weeks (P<0.05). The degree of islet cell autophagy was potentially regulated by the levels of FFA and islet cell insulin and glucagon, which may have been due to the effects of Beclin1/BCL2. [ABSTRACT FROM AUTHOR]

Tebuconazole is widely used as fungicide and has frequently been detected at elevated concentrations in environmental media. To characterize the potential toxicity of tebuconazole on vertebrate and humans. Using zebrafish as a vertebrate model, the toxic effects in liver that produced by low-toxic concentrations of tebuconazole were assessed in adult zebrafish. We further focused on tebuconazole-induced toxicity and its possible mechanism in larval zebrafish using a hepatotoxicity assay. The induction of oxidative stress in adult fish was evaluated by superoxide dismutase (T-SOD), catalase (CAT), peroxidase (POD), glutathione S-transferase (GST) activity, and the increased aspartate aminotransferase (AST)/alanine aminotransferase (ALT) ratio. Significantly increased enzyme activity was observed in the liver of male and female fish at both exposure and depuration stage. Exposure to maximum non-lethal (MNLC) concentration of tebuconazole from 72 to 120 h post-fertilization (hpf) affected the liver size and yolk retention in larval zebrafish. Decreased fluorescence intensity was observed in larval Tg(Apo14:GFP) zebrafish, indicating liver degeneration after tebuconazole treated. Histopathological examination confirmed the alterations in liver histoarchitecture in exposed zebrafish. Significant 1.28-fold and 1.65-fold increases in reactive oxygen species levels were observed in juveniles exposed to MNLC and lethal concentration 10 (LC 10) group, respectively. The acridine orange staining assay showed that apoptotic cells occurred in the liver regions. These results indicated that tebuconazole exposure resulted in impacts on the ecological risk in fish and vertebrate. Overall, the present study suggested further research in needed to better understand the tebuconazole-induced toxicity mechanism that associated with oxidative stress. Image 1 • Tebuconazole induced hepatotoxicity in both adult and larval zebrafish. • Tg(Apo14: GFP) zebrafish was used for hepatotoxicity assay. • Histopathological results showed alterations in liver histoarchitecture after exposure. • ROS-mediated pathway might induce apoptosis in zebrafish after tebuconazole exposure. [ABSTRACT FROM AUTHOR]