<i>Arf</i>
            tumor suppressor and miR-205 regulate cell adhesion and formation of extraembryonic endoderm from pluripotent stem cells

Li, Chunliang; Finkelstein, David; Sherr, Charles J.

doi:10.1073/pnas.1302184110

Cited by 31 publications

(36 citation statements)

References 49 publications

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“…The frequencies of TALEN-induced mutations per number of GFP ϩ transfected clones examined by nucleotide sequencing were 83% for Agouti, 52% for miR-205, and 79% for Arf. When suspended to form embryoid bodies (EBs), Arf-null ES cells exhibit a significant temporal delay in generating extraembryonic endoderm, a defect that is rescued by enforced overexpression of miR-205 (28). Similar delays in forming extraembryonic endoderm were observed in EBs containing biallelic TALEN-inactivated Arf or miR-205 genes, confirming the expected phenotypic consequences of gene inactivation.…”

Section: Methodssupporting

confidence: 59%

“…Pilot studies with ES cells. The 129/SvJ ES cell line F12, derived by Jacqueline Surtel (St. Jude Children's Research Hospital) was routinely expanded on gelatin-coated culture dishes in ES cell medium as described previously (28). Wild-type F12 ES cells were plated into single wells of a six-well culture dish (Corning).…”

Section: Methodsmentioning

confidence: 99%

“…Previous studies revealed that embryoid bodies derived from ES cells lacking the Arf tumor suppressor gene are significantly retarded in generating extraembryonic endoderm but that this defect can be rescued by enforced expression of a single microRNA, miR-205 (28). Based on these observations, we constructed TALEN pairs targeting miR-205 and Arf (see Fig.…”

Section: Talen-induced Mutation Of the Agouti Gene In Zygotesmentioning

confidence: 99%

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Simultaneous Gene Editing by Injection of mRNAs Encoding Transcription Activator-Like Effector Nucleases into Mouse Zygotes

Singleterry

et al. 2014

Molecular and Cellular Biology

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Injection of transcription activator-like effector nucleases (TALEN) mRNAs into mouse zygotes transferred into foster mothers efficiently generated founder mice with heritable mutations in targeted genes. Immunofluorescence visualization of phosphorylated histone 2A (␥H2AX) combined with fluorescence in situ hybridization revealed that TALEN pairs targeting the Agouti locus induced site-directed DNA breaks in zygotes within 6 h of injection, an activity that continued at reduced efficiency in twocell embryos. TALEN-Agouti mRNAs injected into zygotes of brown FvB ؋ C57BL/6 hybrid mice generated completely black pups, confirming that mutations were induced prior to, and/or early after, cell division. Founder mice, many of which were mosaic, transmitted altered Agouti alleles to F 1 pups to yield an allelic series of mutant strains. Although mutations were targeted to "spacer" sequences flanked by TALEN binding sites, larger deletions that extended beyond the TALEN-binding sequences were also detected and were similarly inherited through the germ line. Zygotic coinjection of TALEN mRNAs directed to the Agouti, miR-205, and the Arf tumor suppressor loci yielded pups containing frequent and heritable mutations of two or three genes. Simultaneous gene editing in zygotes affords an efficient approach for producing mice with compound mutant phenotypes, bypassing constraints of conventional mouse knockout technology in embryonic stem cells.

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Section: Methodssupporting

confidence: 59%

Section: Methodsmentioning

confidence: 99%

Section: Talen-induced Mutation Of the Agouti Gene In Zygotesmentioning

confidence: 99%

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Simultaneous Gene Editing by Injection of mRNAs Encoding Transcription Activator-Like Effector Nucleases into Mouse Zygotes

Singleterry

et al. 2014

Molecular and Cellular Biology

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“…Notably, the p19 ARF tumour suppressor, but not p16 INK4A , is concordantly expressed in the proliferating embryonic visceral endoderm and extra-embryonic yolk sac 151 . Presumably, the early embryonic expression of these markers in these tissues connotes a senescence-independent process.…”

Section: Combining Senescence Markersmentioning

confidence: 99%

Forging a signature of in vivo senescence

2015

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'Cellular senescence', a term originally defining the characteristics of cultured cells that exceed their replicative limit, has been broadened to describe durable states of proliferative arrest induced by disparate stress factors. Proposed relationships between cellular senescence, tumour suppression, loss of tissue regenerative capacity and ageing suffer from lack of uniform definition and consistently applied criteria. Here, we highlight caveats in interpreting the importance of suboptimal senescence-associated biomarkers, expressed either alone or in combination. We advocate that more-specific descriptors be substituted for the now broadly applied umbrella term 'senescence' in defining the suite of diverse physiological responses to cellular stress.

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“…Overexpression of CENPF was observed in naive PCa specimens and expression of CENPF acted as an oncogenic gene in PCa cells [22]. Initially, overexpression of miR-205-5p was observed in endoderm and ectoderm in embryonic germ cells and its function was involved in the differentiation and maintenance of epithelium [32]. Expression of miR-205-5p might play a pivotal role in the prevention of the epithelial-mesenchymal transition (EMT) process in epithelial cells.…”

Section: Discussionmentioning

confidence: 99%

Regulation of HMGB3 by antitumor miR-205-5p inhibits cancer cell aggressiveness and is involved in prostate cancer pathogenesis

et al. 2017

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Our recent determination of a microRNA (miRNA) expression signature in prostate cancer (PCa) revealed that miR-205-5p was significantly reduced in PCa tissues and that it acted as an antitumor miRNA. The aim of this study was to identify oncogenic genes and pathways in PCa cells that were regulated by antitumor miR-205-5p. Genome-wide gene expression analyses and in silico miRNA database searches showed that 37 genes were putative targets of miR-205-5p regulation. Among those genes, elevated expression levels of seven in particular (HMGB3, SPARC, MKI67, CENPF, CDK1, RHOU, and POLR2D) were associated with a shorter disease-free survival in a large number of patients in the The Cancer Genome Atlas (TCGA) database. We focused on high-mobility group box 3 (HMGB3) because it was the most downregulated by ectopic expression of miR-205-5p in PC3 cells and its expression was involved in PCa pathogenesis. Luciferase reporter assays showed that HMGB3 was directly regulated by miR-205-5p in PCa cells. Knockdown studies using si-HMGB3 showed that expression of HMGB3 enhanced PCa cell aggressiveness. Overexpression of HMGB3/HMGB3 was confirmed in naive PCa and castration-resistant PCa (CRPC) clinical specimens. Novel approaches to analysis of antitumor miRNAregulated RNA networks in PCa cells may provide new insights into the pathogenic mechanisms of the disease.

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Arf tumor suppressor and miR-205 regulate cell adhesion and formation of extraembryonic endoderm from pluripotent stem cells

Cited by 31 publications

References 49 publications

Simultaneous Gene Editing by Injection of mRNAs Encoding Transcription Activator-Like Effector Nucleases into Mouse Zygotes

Simultaneous Gene Editing by Injection of mRNAs Encoding Transcription Activator-Like Effector Nucleases into Mouse Zygotes

Forging a signature of in vivo senescence

Regulation of HMGB3 by antitumor miR-205-5p inhibits cancer cell aggressiveness and is involved in prostate cancer pathogenesis

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