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@#[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.
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Objective To investigate the effects of lovastatin on inducing G1 phase synchromzation in HEC-1-A cells and examine the cell cycle progression after desynchronization.Methods The doubling time of HEC-1-A cells was detected by cell counting Kit-8 assay.To determine the best lovastatin concentration of G1 synchronization,HEC-1-A cells were treated with lovastatin at concentration of 10,20,30 and 40 μmol/L respectively for 1 × doubling time,and the cell cycle was detected by flow cytometry (FCM).To determine the best period of lovastatin treatment to achieve G1 synchronization,HEC-1-A cells were treated with lovastatin at the best concentration for 0.5 × to 2 × doubling time,and the cell cycle was detected every 4 h using FCM.Furthermore,the cell cycle progress of HEC-1-A cells after desynchronization was also observed.Results The doubling time of HEC-1-A cells was 24 h.Treated with lovastatin at concentration of 40 μmol/L for 28 h achieved maximum G1 arrest (87.87±0.70) ％ in HEC-1-A cells.Minimum G1 phase (58.42±0.54) ％ and maximum S phase (33.58±0.62) ％ were observed after desynchronizing for 20 h.Conclusion Maximum G1 synchronization of HEC-1-A cells is induced by lovastatin at concentration of 40 μmol/L for 28 h.The HEC-1-A cells show minimum G1 phase and maximum S phase after desynchronizing for 20 h.