Background & Aims: Recent genomic studies have identified frequent mutations of AT-rich interactive domain 2 (ARID2) in hepatocellular carcinoma (HCC), but it is not still understood how ARID2 exhibits tumor suppressor activities. Methods: We established the ARID2 knockout HCC cell lines by using CRISPR/Cas9 system, and investigated the gene expression profiles and biological functions. Results: Bioinformatic analysis indicated that UV-response genes were negatively regulated in the ARID2-KO cells, and they were certainly sensitized to UV irradiation. ARID2 depletion attenuated nucleotide excision repair (NER) of DNA damage sites introduced by exposure to UV as well as chemical compounds known as carcinogens for HCC, benzo[a]pyrene and FeCl3, since XPG could not be accumulated without ARID2. By using large-scale public data sets, we validated that ARID2 knockout could lead to similar molecular changes between in vitro and in vivo, and moreover observed a higher number of somatic mutations in the ARID2-mutated subtypes than that in the ARID2 wild-type across various types of cancers including HCC. Conclusions: We provided evidence that ARID2 knockout could contribute to disruption of NER process through inhibiting the recruitment of XPG, resulting in susceptibility to carcinogens and potential hypermutation. These findings have far-reaching implications for therapeutic targets in cancers harboring ARID2 mutations.
Classification of primary liver cancer with immunosuppression mechanisms and correlation with genomic alterations.
Specimen part
View SamplesWe characterized the Drosophila third instar eye disc using single cell RNA-seq and labelled the multiple cell populations. The results identified a novel transcriptional switch in photoreceptors relating to axonal projections. We then performed single cell RNA-seq on rbf (Rb) mutants and compared the results to the WT cell populations. This identified a specific cell population only in the Rb mutant tissue. This cell population has an upregulation of HIF1A and glycolitic genes such as Aldolase and Lactate dehydrogenase. As a result these cells produce lactate and undergo apoptosis. We also show this process to be directly regulated by E2F/Dp. The paper uncovers a novel metabolic aspect of Rb/E2F dependent apoptosis. Overall design: examining WT and Rb mutants third instar eye disc using single cell RNA-seq
Single cell RNA-sequencing identifies a metabolic aspect of apoptosis in Rbf mutant.
Specimen part, Subject
View SamplesInrauterine growth restriction was induced by chronic hyper insulinemia in pregnant rats and differential gene expression was studied using affymetrix rat genome RAE230A.Data was analysed using SAM.
Adult hypertension in intrauterine growth-restricted offspring of hyperinsulinemic rats: evidence of subtle renal damage.
No sample metadata fields
View SamplesBackground: 2,5-Dimethyl-4-hydroxy-3(2H)-furanone (DMHF) is one of the major odor compounds generated by the Maillard reaction. We previously reported that the inhalation of DMHF decreased systolic blood pressure via the autonomic nervous system in rats. The autonomic nervous system is also closely related to appetite regulation. The present study investigated the effects of DMHF on dietary intake and gene expression.
DMHF (2,5-dimethyl-4-hydroxy-3(2H)-furanone), a volatile food component generated by the Maillard reaction, promotes appetite and changes gene expression in the rat brain through inhalation.
Sex, Age, Specimen part, Treatment
View SamplesA triclosan-ciprofloxacin cross-resistant mutant strain of Staphylococcus aureus displays an alteration in the expression of several cell membrane structural and functional genes.
A triclosan-ciprofloxacin cross-resistant mutant strain of Staphylococcus aureus displays an alteration in the expression of several cell membrane structural and functional genes.
No sample metadata fields
View SamplesThe etiology of trauma-hemorrhage shock-induced acute lung injury has been difficult to elucidate due, at least in part, to the inability of in vivo studies to separate the non-injurious pulmonary effects of trauma-hemorrhage from the tissue injurious ones. To circumvent this in vivo limitation, we utilized a model of trauma-hemorrhagic shock (T/HS) in which T/HS-lung injury was abrogated by dividing the mesenteric lymph duct. In this way, it was possible to separate the pulmonary injurious response from the non-injurious systemic response to T/HS by comparing the pulmonary molecular response of rats subjected to T/HS which did and did not develop lung injury as well as to non-shocked rats. Utilizing high-density oligonucleotide arrays and treatment group comparisons of whole lung tissue collected at 3 hours after the end of the shock or sham-shock period, 139 of the 8,799 assessed genes were differentially expressed.
Molecular signatures of trauma-hemorrhagic shock-induced lung injury: hemorrhage- and injury-associated genes.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Molecular pathways reflecting poor intrauterine growth are found in Wharton's jelly-derived mesenchymal stem cells.
Specimen part
View SamplesIn order to identify gene-expression patterns in mesenchymal stem cells associated with different birth weights and intrauterine growth parameters,
Molecular pathways reflecting poor intrauterine growth are found in Wharton's jelly-derived mesenchymal stem cells.
Specimen part
View SamplesIn order to identify gene-expression patterns in mesenchymal stem cells associated with different birth weights and intrauterine growth parameters,
Molecular pathways reflecting poor intrauterine growth are found in Wharton's jelly-derived mesenchymal stem cells.
Specimen part
View SamplesIn order to identify gene-expression patterns in mesenchymal stem cells associated with different birth weights and intrauterine growth parameters,
Molecular pathways reflecting poor intrauterine growth are found in Wharton's jelly-derived mesenchymal stem cells.
Specimen part
View Samples