Loss of <scp>ADAR</scp>1 in human <scp>iPS</scp> cells promotes caspase3‐mediated apoptotic cell death

Katayama, Shota; Shimoda, Kaori; Takenaga, Yuji

doi:10.1111/gtc.12261

Cited by 13 publications

(13 citation statements)

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“…ADAR1-deficiency did not alter cell morphology, alkaline phosphatase (AP) staining activities and the expression levels of pluripotent marker genes, indicating that ADAR1 is not required for maintenance of pluripotency [6] . Furthermore, in vitro differentiation assay revealed that ADAR1 deficient iPS cells could differentiate into three germ layers in vitro [6] .…”

Section: Research Highlightmentioning

confidence: 99%

“…Furthermore, in vitro differentiation assay revealed that ADAR1 deficient iPS cells could differentiate into three germ layers in vitro [6] .…”

Section: Research Highlightmentioning

confidence: 99%

“…In order to analyze functional roles of ADAR1 in human iPS cells, we performed knockdown experiments and evaluated the quality as pluripotent stem cells [6] . ADAR1 deficient iPS cells show a remarkably repressed cell number.…”

mentioning

confidence: 99%

“…To determine whether reduction in cell viability after ADAR1-deficiency was due to induction of apoptosis, apoptotic assays were performed [6] . Annexin V staining assay revealed that remarkable increase in number of apoptotic cells.…”

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confidence: 99%

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RNA editing enzyme ADAR1 in human iPS cells

2015

Stem Cell Transl Investig

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Adenosine deaminases acting on RNA (ADARs) are enzymes related in RNA editing that converts adenosine residues to inosine specifically in double-stranded RNAs. ADAR regulates mRNA stability and gene expression. ADAR1-Dicer complexes promote microRNA processing and RNA interference (RNAi) gene silencing. ADAR1 is highly expressed in human pluripotent stem cells. Recently, we observed that ADAR1-deficiency in human iPS cells promotes caspase3-mediated apoptotic cell death. On the other hand, ADAR1-deficiency did not alter cell morphology, alkaline phosphatase (AP) staining activities and the expression levels of pluripotent marker genes, indicating that ADAR1 is not required for maintenance of pluripotency. Further, ADAR1 deficient iPS cells did not change proliferation rate. Altogether, we demonstrated that ADAR1 is necessary for existence of human iPS cells.

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Section: Research Highlightmentioning

confidence: 99%

“…Furthermore, in vitro differentiation assay revealed that ADAR1 deficient iPS cells could differentiate into three germ layers in vitro [6] .…”

Section: Research Highlightmentioning

confidence: 99%

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confidence: 99%

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RNA editing enzyme ADAR1 in human iPS cells

2015

Stem Cell Transl Investig

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“…11 In addition, loss of ADAR1 in human induced pluripotent stem cells (iPS) promotes caspase3 -mediated apoptotic cell death, which is consistent with the necessity of ADAR1 in iPS cell survival. 12 The fact that downregulation of ADAR1 inhibits cell growth leads to the hypothesis that overexpression of ADAR1 would promote cell proliferation. In this study, we aim to analyze the proteomic effect of ADAR1 overexpression in HEK293 cells using liquid chromatography-tandem mass spectrometry (LC-MS/MS) followed by label-free protein quantification.…”

Section: Introductionmentioning

confidence: 99%

Unraveling molecular effects of ADAR1 overexpression in HEK293T cells by label-free quantitative proteomics

et al. 2016

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ADAR1 is a double-stranded RNA (dsRNA) editing enzyme that specifically converts adenosine to inosine. ADAR1 is ubiquitously expressed in eukaryotes and participate in various cellular processes such as differentiation, proliferation and immune responses. We report here a new proteomics study of HEK293T cells with and without ADAR1 overexpression. The up-and down-regulated proteins by ADAR1 overexpression are identified by liquid chromatography-tandem mass spectrometry (LC-MS/MS) followed by label-free protein quantification. Totally 1,495 proteins (FDR < 0.01) are identified, among which 211 are up-and 159 are down-regulated for at least 1.5-fold (n D 3, p < 0.05). Gene ontology analysis reveals that these ADAR1-regulated proteins are involved in protein translation and cell cycle regulation. Bioinformatics analysis identifies a closely related network consistent for the protein translation machinery and a tightly connected network through proliferating cell nuclear antigen (PCNA)-interactions. Up-regulation of the proteins in the PCNA-mediated cell proliferation network is confirmed by Western blotting. In addition, ADAR1 overexpression is confirmed to increase cell proliferation in HEK293T cells and A549 cells. We conclude that ADAR1 overexpression modulates the protein translation and cell cycle networks through PCNA-mediated protein-protein interaction to promote cell proliferation in HEK293 cells.

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MiR-548c-3p inhibits the proliferation, migration and invasion of human breast cancer cell by targeting E2F3

Tan

Wen

et al. 2020

Cytotechnology

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has been reported to be involved in a variety of tumor processes, but its function in breast cancer remains unclear. In this study, we found that miR-548 was low expressed in breast cancer tissues and cells compared with normal control. We then examined whether up-regulation of miR-548 could improve the progression of breast cancer.Our results indicate that up-regulation of miR-548 significantly inhibits cell proliferation, migration andinvasion, and induces apoptosis in breast cancer cells. Further studies showed that miR-548 could specifically inhibit E2F3 expression. Moreover, rescue test showed that up-regulation of E2F2 could reverse the effect of miR-548 on proliferation, migration, invasion and apoptosis of breast cancer cells. In general, miR-548 could improve the progression of breast cancer. By targeting E2F2, which may make a potential target for the treatment of breast cancer.

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Loss of ADAR1 in human iPS cells promotes caspase3‐mediated apoptotic cell death

Cited by 13 publications

References 15 publications

RNA editing enzyme ADAR1 in human iPS cells

RNA editing enzyme ADAR1 in human iPS cells

Unraveling molecular effects of ADAR1 overexpression in HEK293T cells by label-free quantitative proteomics

MiR-548c-3p inhibits the proliferation, migration and invasion of human breast cancer cell by targeting E2F3

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