Recent advancements in genomic and computational technologies have identified numerous untranslated noncoding transcripts including long noncoding RNAs (lncRNAs) in the human genome. Subsequently, the abundance and functional diversity of lncRNAs have been characterized in cellular and pathological pathways of various diseases and cancer. The transcription factor MYC is one of the most pivotal oncogenes, and the oncogenic pathways of MYC have been thought to be competently elucidated. However, recent studies implicating lncRNAs in the MYC pathways show that our research endeavors and knowledge to this day do not thoroughly elaborate the MYC pathways in cancer. It has been shown in recent studies that lncRNAs employ novel mechanisms to tune MYC activity and orchestrate MYC pathways. Furthermore, a number of lncRNAs that have not been dissected have been profiled and identified in the oncogenic MYC pathways. Thus, the research focusing on lncRNAs provides novel biological knowledge of the MYC pathways and will eventually lead to new potential biomarkers and therapeutic targets in MYC-driven cancers. This review discusses the various functional mechanisms of MYC-associated lncRNAs in MYC activity and MYC pathways.

The propagation of epigenetic information across cell divisions is crucial to the maintenance of cell identity. During DNA replication, both parental and newly synthesized histones are deposited onto the replicating DNA, where they assemble into nucleosomes. Parental histones bear a variety of post-translational modifications, which constitute crucial epigenetic information, and the pattern of parental and newly synthesized histone allocation is crucial for the determination and maintenance of cell fate in multicellular organisms. The DNA replication-coupled nucleosome assembly process is regulated by multitude of histone chaperones, and recent breakthroughs in next-generation sequencing and super-resolution imaging methods have provided novel insights into the underlying mechanisms. Here, we review recent findings concerning parental histone deposition onto replicating DNA strands and the segregation of these to symmetrically or asymmetrically dividing daughter cells. Furthermore, we discuss the role of the allocation patterns of parental and newly synthesized histones in the determination of cell fate.

In mammals, DNA methyltransferases create 5-methylcytosines (5mC) predominantly at CpG dinucleotides. 5mC oxidases convert 5mC in three consecutive oxidation steps to 5-hydroxymethylcytosine (5hmC), 5-formylcytosine (5fC) and then 5-carboxylcytosine (5caC). Upon irradiation with UV light, dipyrimidines containing C, 5mC and 5hmC are known to form cyclobutane pyrimidine dimers (CPDs) as major DNA photolesions. However, the photobiology of 5fC and 5caC has remained largely unexplored. Here, we tested a series of oligonucleotides with single or multiple positions carrying cytosine (C), 5mC, 5hmC, 5fC, or 5caC and irradiated them with different sources of UV irradiation. Although UVC radiation produced CPDs near dipyrimidines containing all types of modified cytosine bases, UVB radiation produced by far the highest levels of CPDs near 5caC-containing sequences. Dipyrimidines one or two nucleotide positions adjacent to 5caC but not always those involving this modified base directly were the major sites for these prominent UVB photoproducts. This selectivity did not depend on whether 5caC was present on one or both DNA strands at CpG sequences. We also observed a tendency of the 5caC-containing DNA strands to undergo apparent covalent crosslinking. This reaction occurred with UVB or UVC, but not with UVA irradiation. Our data show that 5-carboxylcytosine, although generally a rare base in the genome, can nonetheless make a strong contribution to sequence-specific DNA damage perhaps by acting as a DNA-intrinsic photosensitizer.