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Targeting 14-3-3ζ overcomes resistance to EGFR-TKIs in lung adenocarcinoma via BMP2/Smad/ID1 signaling

ABSTRACT: Targeting 14-3-3ζ overcomes resistance to EGFR-TKIs in lung adenocarcinoma via BMP2/Smad/ID1 signaling

PROVIDER: PRJNA657881 | ENA |

REPOSITORIES: ENA

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Targeting 14-3-3ζ overcomes resistance to EGFR-TKIs in lung adenocarcinoma via BMP2/Smad/ID1 signaling

Project description:14-3-3ζ has been found to promote the proliferation, metastasis and chemoresistance of cancer cells in several cancers including lung adenocarcinoma; however, its significance in epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) resistance remains unknown. Our work uncovers a hitherto unappreciated role of 14-3-3ζ in EGFR-TKI resistance. We determined global gene expression profiling in EGFR-TKI-resistant H1975 cells using microarray analysis.

2020-09-30 | GSE156435 | GEO

The BMP2/SMAD pathway is a key regulator of TP53-altered erytholeukemia

Project description:The BMP2/SMAD pathway is a key regulator of TP53-altered erytholeukemia

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Targeting 14-3-3? Overcomes Resistance to Epidermal Growth Factor Receptor-Tyrosine Kinase Inhibitors in Lung Adenocarcinoma via BMP2/Smad/ID1 Signaling.

Project description: Not available

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Epigenetic regulation of Bmp2 and Smad6 in Ras-induced senescence

Project description:Epigenetically silenced Ink4a-Arf locus is activated by loss of H3K27me3 in cellular senescence, where secreted factor expression is also involved. Here we analyzed epigenome and transcriptome alteration during Ras-induced senescence using mouse embryonic fibroblast (MEF). Seventeen genes with H3K27me3 loss and H3K4me3 gain showed marked upregulation, including p16Ink4a and Bmp2, a secreted factor for BMP/SMAD signal. Smad6, specific BMP/SMAD pathway inhibitor, was identified as the only one gene showing de novo H3K27 trimethylation with H3K4me3, resulting in strong repression. Ras-activated cells senesced with SMAD1/5/8 phosphorylation, and they escaped from senescence with decreased SMAD1/5/8 phosphorylation when introducing Smad6 or knocking-down Bmp2.

2011-12-22 | GSE18125 | GEO

The BMP2/SMAD pathway is a key regulator of TP53-altered erytholeukemia [scRNA-seq]

Project description:The BMP2/SMAD pathway is a key regulator of TP53-altered erytholeukemia [scRNA-seq]

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Quantitative analysis of Id1 Wild Type and Id1 knockout hematopoietic stem cells transcriptome

Project description:To explore the molecular basis by which Id1 loss promotes HSC quiescence under stress we compared the transcriptome of Id1-/- and Id1+/+ HSCs isolated from primary BMT recipient mice by RNA-seq. We found 179 upregulated and 1476 downregulated genes in Id1-/- HSCs compared to Id1+/+ HSCs using a fold-change cut-off of 2 . Collectively, the IPA analysis shows that Id1-/- HSCs have gene expression profiles consistent with reduced response to stress, reduced cycling and proliferation, and reduced ribosomal biogenesis and protein synthesis, which is consistent with our hypothesis that Id1-/- HSCs have molecular signature of quiescent HSCs compared to Id1+/+ HSCs.

2018-08-09 | GSE114533 | GEO

The BMP2/SMAD pathway is a key regulator of TP53-altered erytholeukemia [Bulk RNA-seq]

Project description:The BMP2/SMAD pathway is a key regulator of TP53-altered erytholeukemia [Bulk RNA-seq]

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A fine-tuned regulation of Bmp2 by Nodal/TGFβ signalling induced lncRNA-Smad7

Project description:The transforming growth factor beta (TGF-β) superfamily proteins are potent regulators of cellular development and differentiation. Long non-coding RNAs (lncRNAs) play widespread roles in spatial-temporal regulation of early development. However, the roles of lncRNAs regulated by nodal/TGF-β signaling is still elusive. Here, we showed a nodal-driven Smad induced lncRNA in mouse embryonic stem cells (mESCs), lncRNA-Smad7, which is divergently transcribed to Smad7, regulates cell fate determination through repressing Bmp2. Depletion of lncRNA-Smad7 dramatically impairs cardiomyocyte differentiation in mESCs. Moreover, LncRNA-Smad7 represses Bmp2 expression and binds at the promoter region of Bmp2. Importantly, knock-down Bmp2 rescues the defect of cardiomyocyte differentiation. Hence, we showed that lncRNA-Smad7 is antagonistic to BMP signaling in mESCs. Furthermore, lncRNA-Smad7 regulates cell fate determination between osteocytes and myocytes formation in C2C12 cells by repressing Bmp2. Thus, we provide new insights regarding the antagonistic effects between nodal/TGF-β and BMP signaling via lncRNA-Smad7.

2022-10-19 | GSE178136 | GEO

Id1 overexpressing BMDC

Project description:Trascriptional profiling by array of bone marrow derived murine cells trasduced with control and Id1-overexpressing vectors to identify genes changes induced by increased expression of the transcriptional regulator Id1

2015-03-31 | E-MTAB-2280 | biostudies-arrayexpress

ID1 and CEBPA coordinate epidermal progenitor cell

Project description:The regulatory circuits that coordinate epidermal differentiation during development are still not fully understood. Here we report that the transcriptional regulator ID1 is enriched in basal epidermal progenitor cells and find ID1 expression to be diminished upon differentiation. In utero silencing of Id1 impairs progenitor cell proliferation, leads to precocious delamination of targeted progenitor cells and enables differentiated keratinocytes to retain progenitor markers and characteristics. Transcriptional profiling suggests ID1 acts by mediating adhesion to the basement membrane while inhibiting spinous layer differentiation. Co-immunoprecipitation reveals ID1 binding to transcriptional regulators of the class I bHLH family. We localize bHLH Tcf3, Tcf4 and Tcf12 to epidermal progenitor cells during epidermal stratification and established TCF3 as a downstream effector of ID1-mediated epidermal proliferation. Finally, we identify crosstalk between CEBPA, a known mediator of epidermal differentiation, and Id1 and demonstrate that CEBPA antagonizes BMP-induced activation of Id1. Our work establishes ID1 as a key coordinator of epidermal development, acting to balance progenitor proliferation with differentiation and unveils how functional crosstalk between CEBPA and Id1 orchestrates epidermal lineage progression.

2022-10-14 | GSE215055 | GEO

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