Cancer cells possess a unique metabolic phenotype, rewiring their metabolic pathways to support energy-intensive and biosynthetic requirements for exuberant proliferation and migration. Attention has focused on the role of microRNAs (miRNAs) in mediating metabolic shifts in cancer cells. miRNAs participate in cancer metabolism reprogramming mainly by directly silencing the expression of specific genes. This review focuses on miRNA regulation of cancer metabolic reprogramming, including glucose, fatty acid and amino acid metabolism, and allows a deeper understanding of importance of miRNAs in tumorigenesis and progression, therefore, providing new avenues for cancer therapy strategy.
Many types of membraneless organelles and related substructures occur in the nucleus and cytoplasm of cells, providing the essential framework for regulating innumerable biological activities. Fundamentally, these consist of RNA–protein (RNP) condensates formed by the process of liquid–liquid phase separation (LLPS). A salient attribute of these structures is their dynamic nature, a characteristic feature which dovetails with their essential roles in signal transduction and stress responses. In this regard, there is increasing evidence that non-coding RNAs serve as catalysts for the formation of LLPS structures. In this review, we summarize the current research in this field, focusing on how microRNAs, long non-coding RNAs, and circular RNAs contribute to the regulation of phase separation in different LLPS structures. In concert with this approach, we also shed new light onto the increasingly apparent role that phase separation plays in disease, particularly cancer. Finally, we lay out the challenges for this research and project how a deeper understanding of RNA-driven phase separation could help advance disease diagnosis and treatment.
Synthetic lethality (SL) describes a situation in which the occurrence of one genetic event maintains cell viability, whereas the co-occurrence of two genetic events lead to cell death. DNA damage response (DDR) pathway represents the most attractive synthetic lethality targets, since genomic instability is a hallmark of cancers due to the accumulation of DNA mutation during the process of DNA damage response. The definition of synthetic lethality will help to target cancer cells precisely and tackle the undruggable targets. In recent years, the success of DNA damage response inhibitors in cancer treatment highlights the potential of this approach. In this review, we will highlight the concept of synthetic lethality, strategy as well as the most recent development in this area.
Genomic instability is one of the hallmarks of tumors that contributes to tumor heterogeneity and drug resistance. Genetically targeted cancer therapy that focused on genome instability has been a direction for tumor treatment of great interest. Synthetic lethality provides a new approach for the treatment of tumor suppressor gene especially DNA damage response pathway mutation-caused cancers that were not considered as a target in traditional genetic treatment previously. Here, we summarize the systematic classification of synthetic lethality and its mechanism which was divided into gene level, including cellular signaling pathway, cell cycle regulation, metabolism, and epigenetic regulation. The goal of this review was to help deepen the understanding of the mechanism of synthetic lethality and guide the direction for exploring the new synthetic lethal relationships.