RESUMO
@#[Abstract] Objective: To investigate the expression level of lncRNA (long non-coding RNA) SNHG1 in endometrial cancer tissues, and to analyze its mechanism of action as well as its clinical significance. Methods: NCBI-GEO and TCGA database were used to analyze the expression level of SNHG1 in endometrial cancer. A total of 53 cases of endometrial cancer tissue samples and 41 cases of normal endometrial tissue samples were collected from January 2016 to March 2019 at Zhongxin Ecocity Hospital of Tianjin Medical University; in addition, endometrial cancer cell lines Ishikawa and HEC-1A as well as normal endometrial ESC cells were also collected for this study. qPCR was used to detect the expression level of SNHG1 in tissues and cells, and its correlation with the clinical characteristics of patients were statistically analyzed. The effect of SNHG1 on cell proliferation and apoptosis of HEC-1A cells was measured by MTT assay and Annexin V/PI double staining Flow cytometry, respectively. The migration and invasion of HEC-1A cells were measured by Transwell assay. StarBase was used to predict the regulatory relationship between SNHG1 and RELA, which was then verified by qPCR and Western blotting. Dual fluorescent reporter gene system and qPCR were adopted to identify the influence of SNHG1 on NF-κB pathway. Results: The expression of SNHG1 was significantly up-regulated in endometrial cancer tissues compared with normal endometrial tissues (P<0.01), and its expression was related to tumor size, TNM staging, histological grade and lymph node metastasis (all P<0.05). The expression level of SNHG1 in Ishikawa and HEC-1A cells was significantly higher than that in ESC cells (all P<0.01). Overexpression of SNHG1 notably promoted the proliferation, migration and invasion and inhibited cell apoptosis of HEC-1A cells. By promoting the expression of RELA, SNHG1 activated the NF-κB pathway and promoted the expressions of downstream gene IL-6 and CCL19 (all P<0.01). Conclusion: Up-regulated SNHG1 in endometrial cancer functions as an oncogene by activating the NF-κB pathway through promoting the RELA expression.
RESUMO
Natural killer (NK) cells are the first line of defense against pathogens of the immune system and also play an important role in resistance against HIV. The activating receptor NKG2C and the inhibitory receptor NKG2A co-modulate the function of NK cells by recognizing the same ligand, HLA-E. However, the role of NKG2A and NKG2C on viral set point and the prediction of HIV disease progression have been rarely reported. In this study, we determined the expression of NKG2C or NKG2A on the surface of NK cells from 22 individuals with primary HIV infection (PHI) stage and 23 HIV-negative normal control (NC) subjects. The CD4+ T cell count and plasma level of HIV RNA in the infected individuals were longitudinally followed-up for about 720 days. The proportion of NKG2C+NKG2A- NK cells was higher in subjects from the low set point group and was negatively correlated with the viral load. In addition, strong anti-HIV activities were observed in NKG2C+ NK cells from the HIV-positive donors. Furthermore, a proportion of NKG2C+NKG2A- NK cells >35.45%, and a ratio of NKG2C/NKG2A >1.7 were predictive for higher CD4+ T cell counts 720 days after infection. Collectively, the experimental results allow us to draw the conclusion that NKG2C+ NK cells might exert an antiviral effect and that the proportion of NKG2C+NKG2A- NK cells, and the ratio of NKG2C/NKG2A, are potential biomarkers for predicting HIV disease progression.
