Emerging evidence suggests that microRNAs are critical regulators of cancer development and progression. MicroRNA-195 has been reported as a cancer-related microRNA in many human cancers. However, the role of microRNA-195 in pancreatic cancer remains largely unknown. Here, we show that microRNA-195 is downregulated in pancreatic cancer tissues and cell line. Also, we show that overexpression of microRNA-195 inhibits the proliferation and invasion of pancreatic cancer cells, whereas suppression of microRNA-195 promotes proliferation and invasion. We show that microRNA-195 directly targets the fatty acid synthase enzyme and negatively regulates the expression of fatty acid synthase. Also, we show that fatty acid synthase expression is inversely correlated with microRNA-195 expression in pancreatic cancer tissues. Moreover, our results show that microRNA-195 inhibits Wnt signaling in pancreatic cancer cells. By restoring fatty acid synthase expression, we were able to reverse the antitumor effects of microRNA-195 in pancreatic cancer cells. Taken together, our findings show that microRNA-195 inhibits pancreatic cancer cell proliferation and invasion by regulating the fatty acid synthase/Wnt signaling pathway, suggesting a tumor suppressive role for microRNA-195 in the development and progression of pancreatic cancer. Thus, inhibiting fatty acid synthase by microRNA-195 may serve as a novel therapeutic approach for the treatment of pancreatic cancer.
We aimed to explore the role of NLRP3 inflammasome in Bifidobacterium longum-regulated visceral hypersensitivity of postinfectious irritable bowel syndrome (PI-IBS). Fifty NIH mice were divided into five groups (n = 10). The visceral sensitivities of PI-2W and PI-8W groups significantly exceeded than those of normal control groups (P < 0.05), which was significantly decreased in PI-B group (P < 0.05). Significantly more IL-18 and IL-1β were expressed in PI-2W and PI-8W groups than those in normal control groups (P < 0.05), which was significantly decreased in PI-B group (P < 0.05). Bifidobacterium longum may down-regulate IL-18 and IL-1β expressions by inhibiting NLRP3 inflammasome and thus reduce the visceral hypersensitivity of PI-IBS.
The dysregulation of miR-137 plays vital roles in the oncogenesis and progression of various types of cancer, but its role in prognosis of gastric cancer patients remains unknown. This study was designed to investigate the expression and prognostic significance of miR-137 in gastric cancer patients after radical gastrectomy. Quantitative real-time PCR (qRT-PCR) was performed to evaluate the expression of miR-137 in human gastric cancer cell lines and tissues in patients with gastric adenocarcinoma. Results were assessed for association with clinical factors and overall survival by using Kaplan-Meier analysis. Prognostic values of miR-137 expression and clinical outcomes were evaluated by Cox regression analysis. The results exhibited that the expression level of miR-137 was decreased in human gastric cancer cell lines and tissues, and down-regulated expression of miR-137 was associated with tumor cell differentiation, N stage, and TNM stage. Decreased miR-137 expression in gastric cancer tissues was positively correlated with poor overall survival of gastric cancer patients. Further multivariate Cox regression analysis suggested that miR-137 expression was an independent prognostic indicator for gastric cancer except for TNM stage. Applying the prognostic value of miR-137 expression to TNM stage III group showed a better risk stratification for overall survival. In conclusion, the results reinforced the critical role for the down-regulated miR-137 expression in gastric cancer and suggested that miR-137 expression could be a prognostic indicator for this disease. In addition, these patients with TNM stage III gastric cancer and low miR-137 expression might need more aggressive postoperative treatment and closer follow-up.
Objective. We previously described that different concentration Nucleobindin-2 (NUCB2)/Nesfatin-1 gradients differently regulated visceral hypersensitivity in irritable bowel syndrome. Therefore, this study is aimed at evaluating the effect of NUCB2/Nesfatin-1 on model rats with chronic visceral hyperalgesia. Methods. Neonatal and mature Sprague-Dawley rats were randomly divided into the healthy control and chronic visceral hyperalgesia model groups. The model was built by combining maternal separation with the acetic acid enema. The models were identified by the distension volume threshold to reach abdominal withdraw reflex AWR score = 3 , histological staining, and myeloperoxidase (MPO) detection. The visceral sensitivity to chronic visceral hyperalgesia was then evaluated. Result. Rats in the model group responded more strongly to pulling stimulation than healthy controls; the distension volume threshold causing AWR3 response in model rats was lower than the control group before NUCB2/Nesfatin-1 intervention. After intervention, the distension volume threshold was significantly lower in the NUCB2/Nesfatin-1 central intervention group than in the NUCB2/Nesfatin-1 peripheral intervention group, and the peak value of external oblique muscle electrical activity was significantly higher. Additionally, compared with the male intervention group, in the female intervention group, the volume threshold was significantly lower and the peak value was higher. Conclusion. NUCB2/Nesfatin-1 could regulate visceral sensitivity in chronic visceral hyperalgesia model rats; its regulatory effect correlated with the type of NUCB2/Nesfatin-1 intervention approaches (central or peripheral) and sex (male or female).
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