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SIRT6 haploinsufficiency induces BRAFV600E melanoma cell resistance to MAPK inhibitors via IGF signaling

ABSTRACT: Through integrated transcriptomic, epigenomic and proteomic analyses, we identified IGFBP2, an insulin growth factor (IGF) binding protein, as a direct SIRT6 target gene. We further show that SIRT6 haploinsufficiency, but not complete knock out of SIRT6 promotes IGFBP2 expression via increased H3K56 acetylation at the IGFBP2 locus allowing melanoma cell survival in the presence of MAPK signaling inhibitors (MAPKi).

ORGANISM(S): Homo sapiens

PROVIDER: GSE102813 | GEO | 2018/08/18

REPOSITORIES: GEO

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SIRT6 haploinsufficiency induces BRAFV600E melanoma cell resistance to MAPK inhibitors via IGF signalling.

Project description: Not available

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Project description:Sirt6, the NAD+-dependent deacetylase, has been described to deacetylate H3K9, H3K18, and H3K56. However, analysis of the acetylation status revealed that loss of Sirt6 caused a massive increase of histone H3K56ac levels but no detectable change of histone H3K9ac and H3K18ac, indicating that SIRT6 is the dominant deacetylase for H3K56ac in muscle stem cells (MuSCs). Further, we investigate genome-wide H3K56ac profiling in the absence of Sirt6 in MuSCs and mouse embryonic stem cells (mESCs) using high throughput sequencing (ChIP-seq).

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Genome-wide H3K56ac profiling after Sirt6 inactivation in MuSCs [ChIP-seq]

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Genome-wide DNA accessibility maps after Sirt6 inactivation in muscle stem cells [ATAC-seq]

Project description:Sirt6, the NAD+-dependent deacetylase, has been described to deacetylate H3K9, H3K18, and H3K56. However, analysis of the acetylation status revealed that loss of Sirt6 caused a massive increase of histone H3K56ac levels but no detectable change of histone H3K9ac and H3K18ac, indicating that SIRT6 is the dominant deacetylase for H3K56ac in muscle stem cells (MuSCs). Further, we investigate genome transposase-accessible chromatin in the absence of Sirt6 in MuSCs using high throughput sequencing (ATAC-seq).

2022-05-13 | GSE168329 | GEO

SIRT6 regulates glucose metabolism and glutamatergic synapse in the mouse retina

Project description:Microarray analysis on total retinal RNA from 15 day old Sirt6 wild-type (WT) and knock-out (KO) mice. The retina is one of the major energy consuming tissues within the body. In this context, synaptic transmission between light-excited rod photoreceptors and downstream ON-bipolar neurons is a highly demanding energy consuming process. Sirtuin 6 (SIRT6), a NAD-dependent deacylase, plays a key role in regulating glucose metabolism. In this study, we demonstrate that SIRT6 is highly expressed in the retina, controlling levels of histone H3K9 and H3K56 acetylation. Notably, despite apparent normal histology, SIRT6 deficiency caused major retinal transmission defects concomitant to changes in expression of glycolytic genes and glutamate receptors, as well as elevated levels of apoptosis in inner retina cells. Our results identify SIRT6 as a critical modulator of retinal function, likely through its effects on chromatin. Microarray analysis of total retinal RNA from 15 day old Sirt6 wild-type (WT) and knock-out (KO) mice with 3 replicates in each condition using the Affymetrix Mouse Gene 2.1 ST array (transcript (gene) version).

2014-07-30 | E-GEOD-56563 | biostudies-arrayexpress

SIRT6 regulates glucose metabolism and glutamatergic synapse in the mouse retina

2014-07-30 | GSE56563 | GEO

Sirt6 study

Project description:This SuperSeries is composed of the following subset Series: GSE13206: Human shSIRT6 TNF-alpha timecourse GSE13207: Mouse Sirt6-/- TNF-alpha timecourse GSE13208: Mouse Sirt6-/- tissues GSE13209: Mouse Sirt6-/- RelA+/- tissues Refer to individual Series

2010-06-24 | E-GEOD-13272 | biostudies-arrayexpress

Expression data from WT SIRT6 and SIRT6 albumin CRE conditional mice

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2010-06-08 | E-GEOD-21965 | biostudies-arrayexpress

LncPRESS1 is a p53-regulated lncRNA that safeguards pluripotency by disrupting SIRT6 mediated de-acetylation of histone H3K56

Project description:Recent evidence suggests that lncRNAs play an integral regulatory role in numerous functions, including determination of cellular identity. We determined global expression (RNA-seq) and genome wide profiles (ChIP-seq) of histone post-translational modifications and p53 binding in human embryonic stem cells (hESCs) undergoing differentiation to define a high-confidence set of 40 lncRNAs, which are p53 transcriptional targets. We focused on lncRNAs, highly expressed in pluripotent hESCs and repressed by p53 during differentiation, to identify lncPRESS1 as a p53-regulated transcript that maintains hESC pluripotency in concert with core pluripotency factors. RNA-seq of hESCs depleted of lncPRESS1 revealed that lncPRESS1 controls a gene network that promotes pluripotency. Further, we found that lncPRESS1 physically interacts with SIRT6 to prevent SIRT6 chromatin localization and maintain high levels of histone H3K56 and H3K9 acetylation at promoters of pluripotency genes. In summary, we describe a novel pluripotency-specific lncRNA that safeguards the hESC state by disrupting SIRT6 activity

2016-12-07 | GSE76023 | GEO

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