We found that the transplantation of Thy1+ cells transiently increased the liver mass by expanding resident small hepatocy-like progenitor cells(SHPCs).
Transplantation of Thy1<sup>+</sup> Cells Accelerates Liver Regeneration by Enhancing the Growth of Small Hepatocyte-Like Progenitor Cells via IL17RB Signaling.
Specimen part
View SamplesMice with MUTYH-null allele (Mutyh+/-, Mutyh-/-) were fed a high-fat/high-cholesterol (HFHC) diet or HFHC + high iron diet. The incidence of liver tumors and histological features of the liver were compared.
MUTYH is associated with hepatocarcinogenesis in a non-alcoholic steatohepatitis mouse model.
Specimen part, Disease, Treatment
View Samplesp63, like its homologue, the tumor suppressor p53, is also able to induce apoptosis in several cancer cell types. p53 family proteins are composed of three characteristic domains which are: 1) an N-terminal transactivation domain (TAD); 2) a central DNA-binding domain (DBD); and 3) an oligomerization domain (OD). In this study, we constructed recombinant adenoviruses containing hybrid genes composed of fragments of p53 and TAp63 genes by connecting coding sequences of their three functional domains. The potency of tumor growth suppression of these hybrid molecules was evaluated using in vitro and in vivo models. One of the p53-p63 hybrid molecules, p63-53O, was observed to be the most potent activator of human cancer cells to apoptosis when compared to the p53, TAp63 or several alternative p53-p63 hybrid molecules. p63-53O hybrid is composed of TAD and DBD of TAp63 and OD of p53. In an effort to identify specific targets regulated by pro-apoptotic hybrid p63-53O, we next performed Affymetrix Genechip analysis and compared expression patterns in a human osteosarcoma cell line Saos-2 transfected separately with Ad-p53, Ad-TAp63 and Ad-p63-53O.
A novel approach to cancer treatment using structural hybrids of the p53 gene family.
Cell line
View SamplesThe p53 family consists of three members, p53, p73, and p63. These proteins share a high degree of amino-acid sequence similarity and major functional domains. The p53 gene, the first member of the family to be identified, is the most frequent target gene for genetic alterations in human cancers. In contrast, p73 and p63 are mainly involved in normal development and differentiation. These differences among the p53 family are likely to depend on activation or repression of different sets of target genes. In this study, to identify targets specifically regulated by p73, we performed microarray analysis and compared expression patterns in a human steosarcoma cell line Saos-2 infected separately with p53 and TAp73beta expressing adenovirus.
p53 family members regulate the expression of the apolipoprotein D gene.
No sample metadata fields
View SamplesAnaplastic lymphoma kinase tyrosine kinase inhibitors (ALK-TKIs) induce a dramatic response in nonsmall cell lung cancer (NSCLC) patients with the ALK fusion gene. However, acquired resistance to ALK-TKIs in lung cancer cells remains an inevitable problem: ALK secondary mutations and bypass pathways have been reported as major resistance mechanisms. In this study, we aimed to discover a novel mechanism of acquired resistance to ALK-TKIs and a strategy to conquer ALK-positive lung cancer. We established three types of ALK-TKI (crizotinib, alectinib and ceritinib)resistant H2228 non-small cell lung cancer cell lines by high exposure and stepwise methods. We found these cells showed a loss of ALK signaling, overexpressed AXL with epithelialmesenchymal transition (EMT), and had cancer stem celllike properties. Similarly, we demonstrated that TGF-1 treated H2228 cells also showed AXL overexpression with EMT features and ALK-TKIresistance. The AXL inhibitor, R428, or HSP90 inhibitor, ganetespib, were effective in reversing ALK-TKIresistance and EMT changes in both ALK-TKIresistant and TGF-1exposed H2228 cells. Progression-free survival of ALK-positive NSCLC patients with AXL overexpression was shorter than that of patients who underwent crizotinib therapy and showed low AXL expression. Thus, we found ALK signaling-independent AXL overexpression and EMT features were commonly involved in intrinsic and acquired resistance to first and second generation ALK-TKIs. This suggests AXL and HSP90 inhibitors may be promising therapeutic drugs to overcome tumor cells in ALK-positive NSCLC patients.
No associated publication
Cell line
View Sampleswe aimed to explore the potential therapeutic effects of human mesenchymal stem cell on severe liver disease
No associated publication
Sex, Specimen part, Cell line
View SamplesAnalyze of RNA expression of Old Fibroblast and Young Fibroblast. Compare RNA expression of Old Fibroblast to RNA expression of Young Fbroblast
No associated publication
Sex, Specimen part
View Sampleswe analysis of sham fibroblast and UVA fibroblast RNA expression using RNA sequencing and compare RNA expression.
No associated publication
Sex, Specimen part
View SamplesWe generate miR-25 KO mice by Cas-9 technology, and run 5 month kidney RNA sequencing.
No associated publication
Sex, Specimen part, Cell line
View SamplesAdult neural stem cells derived from wild type and Sirt1 conditional knockout mice were treated with or without X-ray, the total RNA extracted from these cells were used for RNA sequencing.
No associated publication
Sex, Age, Specimen part, Cell line
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