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A functional SNP rs12718466 in APOA1 promoter modulates gene expression via interaction with SOX7.

Plasma concentration of high-density lipoprotein cholesterol (HDL-C) is among the most important risk factors for coronary artery disease and apolipoprotein A1 (APOA1) is an essential apolipoprotein that constitutes HDL. However, few comprehensive searches have been conducted to identify noncoding functional SNPs around the APOA1 gene. In this study, we report the identification of a functional SNP, rs12718466, which influences hepatocyte-specific APOA1 gene expression. Furthermore, we identified SRY-box transcription factor 7 (SOX7) as the transcription factor interacting with the rs12718466 SNP, using a novel screening method Transcription Factor Expression Library scan, which employs a comprehensive library of mouse transcription factors. SOX7 binding is allele-dependent, with stronger binding to the normal allele leading to increased APOA1 transcription. In vitro experiments in hepatocytes and in vivo experiments in mice confirmed that overexpressing SOX7 increased APOA1 expression, while knocking it down decreased both APOA1 gene expression and plasma HDL-C levels. Our research demonstrates that rs12718466 is a functional SNP that modulates APOA1 gene expression through its interaction with SOX7, thereby affecting plasma HDL-C concentrations.

Humans

Cardiovascular Organoids With Adjustable Endothelial Composition via SOX17-Engineered hPSCs.

Organoids are considered a novel modeling platform for studying human biology and advancing health research. With the ability to demonstrate complex 3D structure and multicellular interactions, organoids have advanced studies in all major organs as a reliable model. In this study, we generated an advanced cardiovascular organoid by using a genome-edited human pluripotent stem cell line with inducible SOX17 expression, enabling controlled endothelial specification, adjustable cell-type composition, and human heart-like morphology. Our organoids recapitulated the cardiotoxic phenotypes of FDA-approved chemotherapeutic doxorubicin, manifesting as decreased cell viability and diminished contractile activity. Cryoinjury-induced myocardial infarction in our organoids led to reduced beating, viability, and α-actinin expression, along with increased fibroblast formation, which were mitigated by Captopril. Lastly, isoproterenol treatment increased peak Ca2+ transient amplitude and shortened APD50 in our organoids, consistent with previously reported β-adrenergic responses. In summary, we established a protocol for generating in vitro 3D cardiovascular organoids with controllable cellular composition and heart-like structures, providing a robust and easy-to-produce platform for future studies of human heart disease.

Humans

Comprehensive Analyses of SOX7 Provide Novel Insights on Its Tumor Suppressor Role and Its Target Genes with Therapeutic Implications in Multiple Myeloma.

Multiple myeloma (MM) is an incurable hematological malignancy. SOX7, located within the recurrently deleted 8p23.1 region in MM, is suggested to act as a tumor suppressor. We characterized SOX7 through genetic, epigenetic, and functional analyses in MM cell lines. SOX7 was frequently silenced due to deletion and/or promoter hypermethylation. Ectopic SOX7 expression in KMS-18 and MM.1S cell lines caused a progressive decline in SOX7-transduced cells and induced G1 cell cycle arrest and/or apoptosis. Although SOX7 re-expression did not enhance bortezomib efficacy, treatment with the pan-histone deacetylase inhibitor panobinostat induced G1 arrest, promoted apoptosis, and increased SOX7 expression in MM.1S cells. Whole-transcriptome sequencing identified G1/S progression-related Wnt/β-catenin pathway genes as major SOX7-regulated targets, while ChIP-Seq analysis revealed widespread genomic SOX7 occupancy in MM.1S. Flow cytometric analysis of permeabilized bone marrow tumor cells from newly diagnosed and relapsed MM patients demonstrated generally low SOX7 protein expression. Collectively, these results indicate that SOX7 functions as a tumor suppressor in MM, and its inactivation promotes cell cycle progression. The anti-myeloma effects of panobinostat in MM.1S cells may be partially mediated through SOX7 induction.

Multiple Myeloma