RESUMEN
Neuropsychiatric disorder-associated disrupted-in-schizophrenia-1 (DISC1) activates Wnt/ß-catenin signaling by inhibiting glycogen synthase kinase 3 beta (GSK3ß) phosphorylation, and may promote neural progenitor cell and pancreatic ß-cell proliferation. The present study found that DISC1 promotes non-small cell lung cancer (NSCLC) cell growth. Western blotting and immunohistochemistry analyses showed that DISC1 was highly expressed in NSCLC cell lines and patient tissues. DISC1 expression was negatively associated with phosphorylated (p-) GSK3ß, but positively correlated with a more invasive tumor phenotype and predicted poor NSCLC patient prognosis. siRNA-mediated DISC1 silencing increased p-GSK3ß expression and decreased expression of ß-catenin and Cyclin D1, while DISC1 upregulation produced the opposite results. DISC1 knockdown also reduced NSCLC cell proliferation rates in vitro. These results suggest that DISC1 promotes NSCLC growth, likely through GSK3ß/ß-catenin signaling, and that DISC1 may function as an oncogene and novel anti-NSCLC therapeutic target.
RESUMEN
BACKGROUND: Cardiovascular diseases (CVDs) are at a badly high-risk of morbidity and mortality in the world. METHODS: Our study was attempted to investigate the cardioprotective role of curcumin. Hearts injury was assessed in isolated hearts and the rats of coronary artery ligated. RESULTS AND CONCLUSIONS: The inhibition of pro-inflammatory cytokines was observed by curcumin in coronary artery ligated rats. ST segment was also reduced by curcumin. Triphenyltetrazolium chloride staining (TTC) staining and pathological analysis were also showed that curcumin could dramatically alleviate myocardial injury. Besides, the results in vitro also demonstrated that curcumin could improved the function of isolated hearts. Besides, the expressions of inflammation-related pathway in both rats and isolated hearts treated with curcumin were significantly decreased. The present study investigated the protective effects of curcumin on myocardial injury and its mechanism.
RESUMEN
Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related mortality worldwide. However, there is a shortage of suitable diagnostic markers for early stages of NSCLC, and therapeutic targets are limited. Right open reading frame (Rio) kinase 2 (RIOK2) and Nin one binding (NOB1) protein are important accessory factors in ribosome assembly and are highly expressed in malignant tumours; moreover, they interact with each other. However, the RIOK2 expression profile and its clinical significance as well as NOB1's mechanism in NSCLC remain unknown. In this study, NSCLC cell lines and 15 NSCLC tumour tissues (paired with adjacent normal lung tissues) were collected for a real-time quantitative PCR (RT-qPCR) analysis. In addition, 153 NSCLC cases and 27 normal lung tissues were used in an immunohistochemical analysis to evaluate the RIOK2 and NOB1 expression profiles, their clinicopathological factors in NSCLC and their correlations with prognoses. RIOK2 and NOB1 were highly expressed in NSCLC cells and tissues, and their expression profiles were significantly associated with the Tumour Node Metastasis (TNM) clinical stage, lymph node metastasis, and differentiation. RIOK2 expression was correlated with NOB1. The results suggested that simultaneously determining the expression of RIOK2 and NOB1 will improve the diagnostic rate in early stages of NSCLC. Moreover, RIOK2 and NOB1 might be potential targets for NSCLC therapy.