FOXP3 and FOXP3-regulated microRNAs suppress SATB1 in breast cancer cells

McInnes, Natasha; Sadlon, Timothy; Brown, Cheryl Y.; Pederson, Stephen; Beyer, Marc; Schultze, Joachim L.; McColl, Shaun R.; Goodall, Gregory J.; Barry, Simon C.

doi:10.1038/onc.2011.293

Cited by 87 publications

(87 citation statements)

References 56 publications

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“…Within the targeting construct, eGFP was directly followed by the 3 0 UTR of Satb1 to enable the regulation of the reporter gene by endogenous miRNAs previously reported to fine-tune Satb1 expression (Supplementary Fig. 1) 18,20 . Assessment of recombination efficacy revealed a 100% success rate in prokaryotes expressing Cre-recombinase ( Supplementary Fig.…”

Section: Generation Of a Targeting Vector For The Murine Satb1 Locusmentioning

confidence: 99%

Efficient genome engineering by targeted homologous recombination in mouse embryos using transcription activator-like effector nucleases

et al. 2014

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Generation of mouse models by introducing transgenes using homologous recombination is critical for understanding fundamental biology and pathology of human diseases. Here we investigate whether artificial transcription activator-like effector nucleases (TALENs)-powerful tools that induce DNA double-strand breaks at specific genomic locations-can be combined with a targeting vector to induce homologous recombination for the introduction of a transgene in embryonic stem cells and fertilized murine oocytes. We describe the generation of a conditional mouse model using TALENs, which introduce double-strand breaks at the genomic locus of the special AT-rich sequence-binding protein-1 in combination with a large 14.4 kb targeting template vector. We report successful germline transmission of this allele and demonstrate its recombination in primary cells in the presence of Cre-recombinase. These results suggest that TALEN-assisted induction of DNA double-strand breaks can facilitate homologous recombination of complex targeting constructs directly in oocytes.

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Section: Generation Of a Targeting Vector For The Murine Satb1 Locusmentioning

confidence: 99%

Efficient genome engineering by targeted homologous recombination in mouse embryos using transcription activator-like effector nucleases

et al. 2014

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“…In contrast, a study of human breast cancer cell lines, ZR-75-1 and MCF-10A, showed that gain-of-function mutant p53 induces expression of miR-155, which inhibits TGF-β signaling by targeting ZNF652 to promote cancer cell invasiveness (Neilsen et al 2013). Moreover, validated miR-155 target transcripts in the context of breast cancer include both tumor-suppressor genes, like CEBP-β, FOXO3a, ZNF652, and VHL, and oncogenes, like BACH1 and SATB1 (Yin et al 2008;Kong et al 2010Kong et al , 2014McInnes et al 2012;Johansson et al 2013;Neilsen et al 2013).…”

Section: Introductionmentioning

confidence: 99%

Double-stranded microRNA mimics can induce length- and passenger strand–dependent effects in a cell type–specific manner

Goldgraben

Russell

Rueda

et al. 2015

RNA

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MicroRNAs are short (17-26) noncoding RNAs driving or modulating physiological and pathological cellular events. Overexpression of miR-155 is pathogenic in B-cell malignancy but was also reported in a number of solid tumors-in particular, in breast cancer, where its role remains unclear and often contradictory. Using representative cell line models, we sought to determine whether the discrepant miR-155 effects in breast cancer could be explained by the heterogeneity of the disease. The growth of six breast cancer cell lines transfected with several miRNA mimics was analyzed. We found MCF-7 cell growth to be inhibited by miR-155 and miR-145 mimics, both 23-nt long, but not by a number of shorter mimics, including a universal commercial negative control. Microarray and Western blot analyses revealed induction of apoptosis, associated with interferon-β after activation of the double-stranded RNA sensor pathway. 3 ′ Trimming of the miRNA mimics to 21 nt substantially reduced their growth-inhibitory potency. Mutating the canonical seed of the miR-155 mimic had no effect on the induced inhibition, which was abolished by mutating the miRNA seed of the artificial passenger strand. A panel of breast cancer cell lines showed a wide range of sensitivities to 23-mer mimics, broadly consistent with the sensitivity of the cell lines to Poly (I:C). We demonstrate two sources for nonspecific in vitro effects by miRNA mimics: duplex length and the artificial passenger strand. We highlight the danger of a universal 21-mer negative control and the importance of using matched seed mutants for reliable interpretation of phenotypes.

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“…Foxp3 tumor suppressor regulates SATB1 expression in breast epithelial cells and downregulates its expression in miRNA-dependent manner (McInnes et al, 2011). Repression of SATB1 has been also identified as a crucial mechanism for the phenotype and function of T(reg) cells.…”

Section: Regulation Of Satb1 Via Stat-6mentioning

confidence: 99%

“…Interestingly, two recent studies have implicated Foxp3 in the regulation of SATB1 McInnes et al, 2011). Foxp3 tumor suppressor regulates SATB1 expression in breast epithelial cells and downregulates its expression in miRNA-dependent manner (McInnes et al, 2011).…”

Section: Regulation Of Satb1 Via Stat-6mentioning

confidence: 99%