Roles of circRNAs in hematological malignancies

Abstract As one of the leading causes of death, hematologic malignancies are associated with an ever-increasing incidence, and drug resistance and relapse of patients after treatment represent clinical challenges. Therefore, there are pressing demands to uncover biomarkers to indicate the development, progression, and therapeutic targets for hematologic malignancies. Circular RNAs (circRNAs) are covalently closed circular-single-stranded RNAs whose biosynthesis is regulated by various factors and is widely-expressed and evolutionarily conserved in many organisms and expressed in a tissue−/cell-specific manner. Recent reports have indicated that circRNAs plays an essential role in the progression of hematological malignancies. However, circRNAs are difficult to detect with low abundance using conventional techniques. We need to learn more information about their features to develop new detection methods. Herein, we sought to retrospect the current knowledge about the characteristics of circRNAs and summarized research on circRNAs in hematological malignancies to explore a potential direction

VISTA: Video Transmission Over a Semantic Communication Approach

No abstract available

A novel role for the ROS-ATM-Chk2 axis mediated metabolic and cell cycle reprogramming in the M1 macrophage polarization

Reactive oxygen species (ROS) play a pivotal role in macrophage-mediated acute inflammation. However, the precise molecular mechanism by which ROS regulate macrophage polarization remains unclear. Here, we show that ROS function as signaling molecules that regulate M1 macrophage polarization through ataxia-telangiectasia mutated (ATM) and cell cycle checkpoint kinase 2 (Chk2), vital effector kinases in the DNA damage response (DDR) signaling pathway. We further demonstrate that Chk2 phosphorylates PKM2 at the T95 and T195 sites, promoting glycolysis and facilitating macrophage M1 polarization. In addition, Chk2 activation increases the Chk2-dependent expression of p21, inducing cell cycle arrest for subsequent macrophage M1 polarization. Finally, Chk2-deficient mice infected with lipopolysaccharides (LPS) display a significant decrease in lung inflammation and M1 macrophage counts. Taken together, these results suggest that inhibiting the ROS-Chk2 axis can prevent the excessive inflammatory activation of macrophages, and this pathway can be targeted to develop a novel therapy for inflammation-associated diseases and expand our understanding of the pathophysiological functions of DDR in innate immunity