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5-methylcytosine was shown before to be an epitranscriptomic mark. Yang et al. now explored the unique topology of this mRNA modification, identified its writer and demonstrated its involvement in nuclear-cytoplasmic shuttling mediated by a specific reader.
High levels of endogenously generated DNA damage drive oncogenesis, sustain malignant progression and increase therapy resistance. In a paper recently published in Cell Research, Liu and colleagues added additional insights into this topic by uncovering a novel intrinsic source of double-strand breaks that fosters the aggressiveness and stemness of malignant cells.
Chemotherapy is a predominant strategy to treat cancer and is often associated with toxicities like severe diarrhea that puts patients at additional risk and can hinder treatment strategies. Lian et al. recently explored the immune-mediated mechanisms of Irinotecan-induced diarrhea in colorectal cancer and found that double-stranded DNA in small vesicles can launch inflammation pathways in immune cells through the cytosolic DNA sensor AIM2.
Circular RNAs (circRNAs) were only recently discovered as a new class of noncoding RNAs, functionally still largely uncharacterized. Three publications that appeared concurrently in Cell Research and Molecular Cell provide initial evidence for certain endogenous circRNAs coding for proteins.
After injury and in disease of the central nervous system (CNS), local cells called astrocytes respond with diverse molecular changes whose functional consequences are incompletely understood. A combined genomic and experimental analysis shows that classically-activated microglia, which are innate immune cells resident in CNS neural tissue, release molecules that drive astrocytes into a neurotoxic state, raising important questions about potential adaptive and maladaptive functions of such a mechanism.
