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Xia Wang,Hongqin Zhao,Shaonan Yang,Xiaojun Shao,Shumin Nie,Xudong Pan 대한독성 유전단백체 학회 2019 Molecular & cellular toxicology Vol.15 No.3
Backgrounds: Metastasis associated lung adenocarcinoma transcript 1 (MALAT1) is an lncRNA that has been suggested as a key regulator in the onset of atherosclerosis (AS). This study described the role of MALAT1 in oxidized low density lipoprotein (ox-LDL)-induced endothelial cells death. Methods: Human umbilical vein endothelial cells (HUVECs) were subjected to ox-LDL, before which the expression of MALAT1 was overexpressed by transfection. CCK-8 assay, flow cytometer detection, and western blot were carried out to evaluate cell viability, apoptosis and autophagy. qRT-PCR and western blot analyses were performed to investigate the regulatory relationship between MALAT1, Matrix Gla protein (MGP) and mTOR signaling to decode the underlying mechanism. Results: Up-regulation of MALAT1 attenuated ox-LDLinduced HUVECs lose, as evidenced by the promoted cell viability, and the decreased apoptosis rate. This finding was coupled with the down-regulated p53, Bax, active-caspase-3, Beclin-1 and LC3-II, as well as the up-regulated Bcl-2 and p62. Meanwhile, MALAT1 upregulation promoted the phosphorylation of p70S6K and mTOR, and the expression of MGP. MGP up-regulation exhibited MALAT1-like propoties in preventing ox-LDL-induced cell death and mTOR deactivation. Of contrast, MGP silence affected HUVECs survival and mTOR signaling resulted in contrary impacts. Conclusion: The present work described that MALAT1 up-regulation prevented ox-LDL-mediated apoptosis and autophagy in HUVECs. The protective effects of MALAT1 might be partially via up-regulating MGP, which led to the activation of mTOR signaling.
Zhiying Xu,Bingyi Yang,Jun Guan,Weiwei Shan,Jiongbo Liao,Wenyu Shao,Xiaojun Chen 대한부인종양학회 2023 Journal of Gynecologic Oncology Vol.34 No.1
Objective: To evaluate the effect of levonorgestrel-releasing intrauterine system (LNG-IUS) plus oral megestrol acetate (MA) as fertility-preserving treatment in patients with early-stage endometrial cancer (EEC). Methods: In this single-center, phase II study with open-label, randomized and controlled design, young patients (18–45 years) diagnosed with primary EEC were screened, who strongly required fertility-preserving treatment. Patients were randomly assigned (1:1) into MA group (160 mg oral daily) or MA (160 mg oral daily) plus LNG-IUS group. Pathologic evaluation on endometrium retrieved by hysteroscopy was performed every 3 months. The primary endpoint was complete response (CR) rate within 16 weeks of treatment. The secondary endpoints were CR rate within 32 weeks of treatment, adverse events, recurrent and pregnancy rate. Results: Between July 2017 and June 2020, 63 patients were enrolled and randomly assigned. Totally 56 patients (26 in MA group; 28 in MA + LNG-IUS group) were included into primary-endpoint analyses. The median follow-up was 31.6 months (range, 3.1–94.0). No significant difference in 16-week CR rate were found between MA and MA + LNG-IUS groups (19.2% vs. 25.0%, p=0.610; odds ratio=1.40; 95% confidence interval=0.38–5.12), while the 32-week CR rates were also similar (57.1% and 61.5%, p=0.743), accordingly. More women in MA + LNG-IUS group experienced vaginal hemorrhage (46.4% vs. 16.1%; p=0.012) compared with MA group. No intergroup difference was found regarding recurrence or pregnancy rate. Conclusion: Compared with MA alone, the addition of LNG-IUS may not improve the early CR rate for EEC, and may produce more adverse events instead.