Chinese PLA General Hospital

About: Chinese PLA General Hospital is a healthcare organization based out in Beijing, China. It is known for research contribution in the topics: Medicine & Population. The organization has 18037 authors who have published 12349 publications receiving 184803 citations. The organization is also known as: 301 Military Hospital.

Methylation‐mediated repression of microRNA 129‐2 enhances oncogenic SOX4 expression in HCC

Abstract: Background & Aims Aberration of miR-129-2 has been linked to a variety of human tumours. However, whether miR-129-2 is involved in hepatocarcinogenesis remains unknown. Here, we investigate the involvement of miR-129-2 in HBV infection-related HCC. Methods A total of 75 paired tumour and their corresponding non-tumour liver tissues from HCC patients with serum HBsAg positive were collected. The methylation of miR-129-2 gene was quantitatively analysed by a DNA methylation-sensitive endonuclease digestion followed by quantitative PCR. The expression of mature miR-129-2 (miR-129-3p) was detected by Taqman RT-PCR. SOX4 expression was detected using quantitative realtime RT-PCR, western blot and immunohistochemical staining. The function of miR-129-2 was investigated using cell proliferation and clonogenicity assays in vitro. Results Compared with the adjacent non-tumour tissues, tumour tissues exhibited significantly increased miR-129-2 hypermethylation both in frequency (37.33% vs. 8%, P < 0.0001) and in intensity (14.77% vs. 3.08%, P = 0.002). Accordantly, miR-129-3p expression in HCC tissues was significantly lower than that in non-tumour tissues (P = 0.0461), in a manner reversely correlated with the level of miR-129-2 hypermethylation. Notably, SOX4 level in the HCC tissues was significantly higher than that in non-tumour tissues (P = 0.0174) and normal liver tissues (P = 0.0077), correlated reversely with miR-129-3p level (P = 0.0105). Furthermore, overexpression of miR-129-2 in HepG2 reduced cell proliferation and clonogenicity, while co-expression with SOX4 could partially reverse its antitumor effects. In addition, SOX4 in HepG2 cell can enhance β-catenin/TCF activity by increasing β-catenin level. Conclusion The current data indicated that methylation-mediated repression of miR-129-2 may enhance oncogenic SOX4 expression and involve in HCC tumorigenesis.

CircHIPK3 promotes proliferation and invasion in nasopharyngeal carcinoma by abrogating miR-4288-induced ELF3 inhibition.

Abstract: Circular RNAs (circRNAs) are reported to regulate the development and progression of multiple cancers. However, the functions of circRNAs in nasopharyngeal carcinoma (NPC) are unclear. In this study, we identified that circular homeodomain interacting protein kinase 3 (circHIPK3) was highly expressed in NPC tissues and cell lines. Moreover, we found that circHIPK3 expression levels could act as a prognostic marker in NPC patients. We showed that circHIPK3 silence repressed NPC cell proliferation, migration, and invasion in vitro. In addition, circHIPK3 depletion dramatically repressed tumor growth and metastasis in vivo. Mechanistically, we revealed circHIPK3 as a competing endogenous RNA of microRNA (miR)-4288 that targets E74-like ETS transcription factor 3 (ELF3) in NPC cells. We found that miR-4288 inhibition reversed the effects of circHIPK3 silence on NPC cells. Furthermore, rescue assays also indicated that circHIPK3 promoted the malignant behaviors of NPC cells via enhancing ELF3 expression by suppressing the miR-4288 levels. In conclusion, our findings demonstrated that circHIPK3 facilitated NPC progression through protecting ELF3 from miR-4288-mediated silencing, which suggested that the circHIPK3-miR-4288-ELF3 regulatory loop might be a potential target for NPC prevention.

Intensive glucose therapy and clinical implications of recent data: a consensus statement from the Global Task Force on Glycaemic Control

Abstract: Background: There is compelling evidence showing that achieving good glycaemic control reduces the risk of microvascular complications in people with type 1 and type 2 diabetes. Likewise, there is clear evidence to show that achieving good glycaemic control reduces the risk of macrovascular complications in type 1 diabetes. The UKPDS 10-year follow up suggests that good glycaemic control also reduces the risk of macrovascular complications in type 2 diabetes. Despite this, recent results from ACCORD, ADVANCE and VADT present conflicting results and data from the ACCORD trial appear to suggest that very low HbA(1c) targets (< 6.0%) may, in fact, be dangerous in certain patient populations. Aim: To review recent results from ACCORD, ADVANCE and VADT and provide clear guidance on the clinical significance of the new data and their implications for the practising physician treating patients with type 2 diabetes. Methods: A Pubmed search was used to identify major randomised clinical trials examining the association between glycaemic control and diabetes-associated complications. The data was reviewed and discussed by the GTF through a consensus meeting. The recommendations for clinical practice in this statement are the conclusions of these analyses and discussions. Results: Evidence from ACCORD, ADVANCE, VADT and UKPDS suggests that certain patient populations, such as those with moderate diabetes duration and/or no pre-existing CVD, may benefit from intensive blood glucose control. These trials highlight the benefit of a multifactorial treatment approach to diabetes. However, ACCORD results indicate that aggressive HbA(1c) targets (< 6.0%) may not be beneficial in patients with existing CVD and a longer duration of diabetes. Conclusions: Glycaemic control remains a very important component of treatment for type 2 diabetes and contrasting results from the ACCORD, ADVANCE and VADT should not discourage physicians from controlling blood glucose levels. (Less)