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DLK1 may constitute a novel diagnostic biomarker and therapeutic target for HGSC.
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DLX6-AS1, combined with miR-129-5p and DLK1, can be utilized as factors for the clinical diagnosis and prognosis of osteosarcoma.
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A direct relationship between DLK1-DIO3 deregulation and replicative senescence of adipose-derived stem cells is reported, involving upregulation of a very significant fraction of its largest miRNA cluster (14q32.31), paralleled by the progressive overexpression of the lncRNA MEG3.
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These results suggest that the DLK1-MEG3 locus, and not the IGF2-H19 locus, drives the tumorigenicity of NT2 cells. Based on these results, we identified DLK1 as a novel treatment target for EC that could be downregulated by 5-azaD.
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Data suggest that targeted methylation of MEG3-DMRs (differentially methylated regions) is sufficient to repress DLK1-MEG3 locus and increase beta-cell susceptibility to cytokines; this study provides evidence for role of novel enhancer in regulation of imprinting at DLK1-MEG3 locus in beta-cells of subjects with type 2 diabetes . (MEG3 = MEG3 non-coding RNA; DLK1 = delta-like 1 protein)
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We conclude methylation changes at some CpG sites of MEST and DLK differentially methylated regions in preeclamptic group
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point mutations in DLK1 and KCNK9 at least do not seem to be a common cause of central precocious puberty in girls.
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The expression of piRNAs encoded at DLK1-DIO3 enhances the prognostic potential of small non-coding RNAs specific to this locus in predicting lung cancer patient outcome.
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targeting DLK1 might inhibit the tumor growth via initiating cell differentiation of hepatocellular carcinoma (HCC) cancer stem cell.
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SASH1 acts through NOTCH1 and its inhibitor DLK1 in a three-dimensional model of lumenogenesis involving CEACAM1.
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The data presented in this work suggest that a fine regulation of NOTCH signaling BY DLK1 plays an important role in the control of breast cancer cell proliferation and invasion.
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results demonstrate that miR-129-5p inhibits non-small cell lung cancer stemness and chemoresistance through direct targeting of DLK1
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A complex defect of DLK1 ( approximately 14-kb deletion and 269-bp duplication) was identified in a family with central precocious puberty. This deletion included the 5' untranslated region and the first exon of DLK1, including the translational start site. Only family members who inherited the defect from their father have precocious puberty, consistent with the known imprinting of DLK1.
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Loss of DLK1 expression is associated with fetal growth retardation complications of pregnancy.
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In neonatal skin, DLK1 exhibited a high degree of monoallelic expression from the paternal allele.
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The study evaluated the roles of extracellular soluble DLK1, comprising six EGF-like domains and juxtamembrane regions, in human pancreatic cancer MIA PaCa-2 cells in vitro and in vivo. Soluble DLK1 exerted antitumor effects not only in cancer cell migration and anchorage-independent cell growth but also in in vivo tumor growth.
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Treatment of mice with recombinant human DLK1 during pregnancy has significant effects on AT of the offspring. This can be associated with counter-regulatory changes in the Notch1 signaling cascade.
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NOTCH1 ligand Delta-like 1 homolog (DLK1) self interacts
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Pref-1 induces insulin synthesis and secretion via two independent pathways
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Data from longitudinal, nested case-control study conducted in rural South Korea suggest that low serum levels of DLK1 (preadipocyte factor 1) may be useful biomarker for identifying women (but not men) at high risk of developing insulin resistance, prediabetes, and type 2 diabetes.
