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Science Papers Present Multi-Omic Analysis of Lung Cells, Regulation of Cardiomyocyte Proliferation

A multi-omic analysis of lung cells performed by a Fred Hutchinson Cancer Research Center-led team has uncovered a key factor involved in lung adenocarcinoma. Having previously identified somatic mutations and amplifications in RIT1 — the gene encoding the RAS family guanosine triphosphatase — in lung adenocarcinomas, the investigators aimed to explore the biological pathways regulated by RIT1 and how they relate to the oncogenic KRAS network. As they describe in Science Signaling this week, they did so by performing quantitative proteomic, phosphoproteomic, and transcriptomic profiling of isogenic lung epithelial cells in which they ectopically expressed wild-type or cancer-associated variants of RIT1 and KRAS. They found that overexpression of wild-type RIT1 partially phenocopied oncogenic RIT1 and KRAS, implicating RIT1 protein abundance in its pathogenic function and suggesting that chromosomal amplification of wild-type RIT1 in lung and other cancers may be tumorigenic. "Together, these results demonstrate the power of quantitative proteomics and transcriptomics to provide global views of oncogene signaling," the study's authors write.

A novel link between heart neurons and clock genes in the regulation of cardiomyocyte proliferation and heart size is demonstrated in a study appearing in this week's Science Advances. Neurons are known to be involved in the regulation of organ development, pathogenesis, and regeneration, but how they influence heart development and regeneration is unclear. To gain insight, Johns Hopkins University investigators genetically inhibited sympathetic Innervation in mouse hearts, resulting in decreased cardiomyocyte proliferation. Follow-on transcriptomic and protein analysis revealed strong downregulation of two clock gene homologs with accompanying upregulation of cell cycle genes. Deletion of the two clock genes increased heart size and cardiomyocyte proliferation, while a pharmacologic increase in sympathetic activity induced expression of the genes and suppressed cardiomyocyte proliferation. "We believe that our study provides novel insights into the role of cardiac sympathetic innervation in regulating clock and cell cycle genes in postnatal hearts," the study's authors write.