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PNAS Studies Look at Lung Cancer LncRNA, Hi-C Clustering, and More

A team from China describes potential ties between lung adenocarcinoma and a long, non-coding RNA called LINC00673-v4. Starting with a luciferase assay, insights gleaned from the Cancer Genome Atlas transcriptome sequencing efforts, and a rapid amplification of cDNA ends experiment, the researchers found a LINC00673 isoform that appeared to influence WNT/beta-catenin signaling in lung adenocarcinoma cells. With a series of follow-up experiments, together with data from the Atlas of Noncoding RNAs in Cancer, they found that LINC00673-v4 was not only found at higher-than-usual levels in lung adenocarcinoma cells, but also appeared to influence the invasiveness of lung cancer cell lines as well as the progression and metastatic potential of lung cancers in a mouse model. "Together," they write, "our data suggest that LINC00673-v4 is a driver molecule for metastasis via constitutively activating WNT/beta-catenin signaling in [lung adenocarcinoma] and may represent a potential therapeutic target against the metastasis of [lung adenocarcinoma]."

Researchers from the Salk Institute for Biological Studies, the University of California, San Diego, and the University of Illinois at Urbana-Champaign present an algorithm called scHiCluster for imputing and clustering Hi-C interaction profiles from single cells. The approach is designed to profile cell type-specific chromosome structures, the team says, and the approach includes imputations made with the help of linear convolution and random walk. By applying scHiCluster to simulated and real single-cell Hi-C data, for example, the authors demonstrate that the approach can bump up the Hi-C clustering accuracy of low-coverage datasets, making it possible to pick up topologically-associating domain-like structures in individual cells.

A Stanford University-led team present epigenetic profiles for self-renewing, stem-like CD8 T immune cells that express both PD-1 and TCF1 proteins, which have been previously documented in mice and humans with chronic infections or certain cancers. Using ATAC-seq, the researchers assessed chromatin accessibility patterns in these stem-like CD8 T cells and in exhausted CD8 T cells, uncovering several apparent regulatory differences between the those immune cell types. From these and other results, including epigenetic profiles in CD8 T cells from mice with chronic infections, the authors conclude that "the chronic stem-like CD8 T cell program represents a specific adaptation of the T cell response to persistent antigenic stimulation."