ABSTRACT
The understanding of DNA-surfactant interactions is important for fundamental physical biology and developing biomedical applications. In the present study, we demonstrated a DNA-surfactant nano-machine model by modulating the compaction of DNA in dodecyldimethylamine oxide (DDAO) solutions. By controlling DDAO concentration and pH of solution, we are able to adjust the compacting force of DNA so as to pull biomolecular subunits connected to it. The pulling force of the machine depends on DDAO concentration and pH of solution, ranging from near zero to about 4.6 pN for 10 mM DDAO concentration at pH = 4. The response time of the machine is about 3 minutes for contracting and 2 minutes for releasing in 5 mM DDAO solution. We found that DDAO has no significant influence on DNA under basic conditions, but compacts DNA under acidic conditions, which is enhanced with decreasing pH of solution. Meanwhile, we found the accompanying charge inversion of DNA in the process of DNA compaction by DDAO.
ABSTRACT
The article entitled, "lncRNA IGF2-AS Promotes Cell Proliferation, Migration, and Invasion of Gastric Cancer by Modulating miR-937/EZH2 Axis," by Zizi Li, Zhanyu Li, Zhijuan Zhong, Jianhui Zhou, Shenhao Huang, Wenying Zhou, and Jianfeng Xu (Cancer Biother Radiopharm epub 25 May 2020; Doi: 10.1089/cbr.2019.3275) is being officially retracted from the literature. The Editor-in-Chief of Cancer Biotherapy and Radiopharmaceuticals (CBR) received an email from the corresponding author of the article, Wenying Zhou, on September 7, 2020, indicating: " this manuscript should no longer be published [because of] information from our superior and also after discussion with my research team, we want to repeat our experiment and then revise the [manuscript]. Our team has a lot of controversy about these results. In order to ensure the quality of the data and not to mislead readers, we decided to [retract] the manuscript. We will be more rigorous in our further study." The editor requested further information about precisely which data could not be reproduced, to which Dr. Wenying Zhou responded: " we found that the results of Figure 4B and 4C, Figure 5A and 5B could not be repeated. Our repeated results of Figure 4B and 4C were as follow[s]: compared with miR-NC group, there was no significant decrease of the luciferase activity in miR-937 group when cells co-transfected with EZH2 3'-UTR-WT. Our repeated results of Figure 5A and 5B were as follow[s]: miR-937 inhibited the proliferation of MNK-28 and SGC-7901 cells, but the cell proliferation had no significant change in miR-937+EZH2 group compared with miR-937+pcDNA group. These findings resulted in the uncertainty of the targeted relationship between miR-937 and EZH2. We also repeated these experiments in different environments, but they all contradict the results in the original data. So, the conclusion is very controversial. In a responsible attitude to the readers, we decide to [retract] the manuscript." The authors have extended their apologies to the Editor and to the readers of CBR. Though in the author's original email, the request was made to "withdraw" the paper, CBR has decided to fully retract it due to irreproducible data, as the journal is committed to preserving the scientific literature and the community it serves.
ABSTRACT
miR-155 plays critical roles in numerous physiological and pathological processes, however, its function in the regulation of blood glucose homeostasis and insulin sensitivity and underlying mechanisms remain unknown. Here, we reveal that miR-155 levels are downregulated in serum from type 2 diabetes (T2D) patients, suggesting that miR-155 might be involved in blood glucose control and diabetes. Gain-of-function and loss-of-function studies in mice demonstrate that miR-155 has no effects on the pancreatic ß-cell proliferation and function. Global transgenic overexpression of miR-155 in mice leads to hypoglycaemia, improved glucose tolerance and insulin sensitivity. Conversely, miR-155 deficiency in mice causes hyperglycemia, impaired glucose tolerance and insulin resistance. In addition, consistent with a positive regulatory role of miR-155 in glucose metabolism, miR-155 positively modulates glucose uptake in all cell types examined, while mice overexpressing miR-155 transgene show enhanced glycolysis, and insulin-stimulated AKT and IRS-1 phosphorylation in liver, adipose tissue or skeletal muscle. Furthermore, we reveal these aforementioned phenomena occur, at least partially, through miR-155-mediated repression of important negative regulators (i.e. C/EBPß, HDAC4 and SOCS1) of insulin signaling. Taken together, these findings demonstrate, for the first time, that miR-155 is a positive regulator of insulin sensitivity with potential applications for diabetes treatment.
