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In this issue, the paper by Yamazaki et al describes how continuous formation of small clusters of LGR5-positive cells contribute to tumor growth in colorectal cancer. The cover shows distribution of LGR5-positive cells (green) and HLA-DMA (red) in 3D structures.
This mini-review summarizes the role of βcysteine 93 in oxidative stability of hemoglobin in human blood. βCys93 has been recognized as an end point for radicals originating from heme during oxidative stress and therefore it may be an important biological marker of oxidative stability of hemoglobin within red blood cells intended for transfusion or in hemoglobinopathies.
This study demonstrates that small clusters (sCLs) of tumor cells with high expression of LGR5 continuously form in the invasive front in a colorectal cancer xenograft model. This structure is characterized by stress response and partial/hybrid epithelial-mesenchymal transition. These sCLs are an important contributor to tumor growth and the expansion of cancer stem cells.
The authors describe a sarcoma with a novel fusion between NUTM1 and MXI1, a member of the MAD gene family. Transcriptome analysis and in vitro studies showed that MXI1-NUTM1 partially phenocopied MYC, providing evidence that MAD family members, normally repressors of MYC activity, can be converted into MYC-like mimics by fusion to NUTM1.
This study demonstrates that NFAT5 promotes oral squamous cell carcinoma progression in the hyperosmotic environment through increased expression of DPAGT1, an essential enzyme for protein glycosylation, and altered EGFR subcellular localization from the cytoplasm to the plasma membrane in tumor cells.
Overexpression of pigment epithelium-derived factor (PEDF) in placenta-derived mesenchymal stem cells (PD-MSCs) improved the mitochondrial activities, and induced regeneration of oxidative stress-damaged RPE through regulating oxidative status and mitochondrial biogenesis. Therefore, genetic modification of PD-MSCs with PEDF might be a new cell therapy for treatment of retinal degenerative diseases.
Ascorbate can act as an oxidant to induce tumor cell death at a pharmacological dose. Here the authors show that this response is associated with increases in GPCR Gi/o activity. This effect promotes rises in intracellular Ca2+ influx through transient receptor potential channel activity in retinoblastoma cells.
Cardiovascular diseases are the leading cause of death worldwide. Myocardial ischaemia/reperfusion (I/R) injury is a major risk for cardiovascular disease. Herein, the authors demonstrate that circPAN3 ameliorates myocardial I/R injury by absorbing miR-421 to regulate Pink1-mediated autophagy, which may provide potential therapeutic targets in I/R injury.
This study describes how miR-221-3p in endothelial cells reduces angiogenesis by inhibiting hypoxia-inducible factor-1α. Because antagonism of miR-221-3p significantly improves the cardiac function of mice with heart failure it may be a new and effective molecular target for progressing and treatment of heart failure.
This study shows in vivo and in vitro evidence to support a novel tree shrew model of lung fibrosis. Tree shrews are genetically, anatomically, and metabolically closer to humans than rodents or dogs; therefore, the tree shrew model presents a unique opportunity for basic and translational research in lung fibrosis.
Photoactivatable-Cre (PA-Cre) knock-in mice was established and characterized for the spatial regulation of Cre recombinase activity with blue light exposure. Spot irradiation or long-term irradiation using a wireless LED could induce locus-specific recombination. The PA-Cre knock-in mice promise a useful resource to elucidate gene function in vivo spatiotemporally.