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Deep Sequencing analysis of the total RNA state and the polyadenylation state of mRNAs in Scrambled or CNOT7 knockdown neurons

ABSTRACT: Differential thermal elution over poly(U) agarose was used to identify mRNAs that underwent a change in their poly(A) tail following CNOT7 knockdown in cultured hippocampal neurons. Total RNA levels were also measured from both sets to identify changes in stability or expressions of mRNAs in the different cell types

ORGANISM(S): Mus musculus

PROVIDER: GSE88777 | GEO | 2016/10/15

SECONDARY ACCESSION(S): PRJNA348541

REPOSITORIES: GEO

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RNA IP Seq analysis of Cnot7 in 4T1 mammary tumor cells

Project description:Native RNA immunoprecipitation of Cnot7-bound transcripts. Abstract: Accumulating evidence supports the role of an aberrant transcriptome as a driver of tumor cell metastatic potential. Deadenylation is a general regulatory node for post-transcriptional control by microRNAs and other determinants of RNA stability. We show here that CCR4-NOT subunit CNOT7 is a deadenylase-dependent driver of tumor cell autonomous metastatic potential. Metastasis promotion by CNOT7 is dependent on contact with CNOT1 and TOB1. We further show TOB1 independently drives metastasis. RNA-immunoprecipitation and integrated transcriptome wide analyses reveal that CNOT7-regulated transcripts are enriched for a tripartite 3’UTR motif bound by RNA-binding proteins known to complex with CNOT7, TOB1, and CNOT1. Collectively, our data support a model of CNOT7, TOB1, CNOT1, and RNA-binding proteins collectively exerting post-transcriptional control on a metastasis suppressive transcriptional program to drive tumor cell metastasis.

2015-09-23 | GSE73366 | GEO

CNOT7 Promotes Radiation Resistance in Colorectal Cancer via XRCC6-Mediated NHEJ DNA Repair Pathway

Project description:In this study, we identified CNOT7 as a key protein influencing the radiotherapy sensitivity of rectal cancer through proteomic sequencing of patient tissues. Patients with high CNOT7 expression often exhibit poorer prognoses during radiotherapy. We explored the potential mechanisms by which CNOT7 affects radiotherapy sensitivity in CRC. CNOT7 reduces polyubiquitination of K48 linked lysine 526 on XRCC6 by regulating TRIM21. This enhances DNA damage repair primarily mediated by the NHEJ pathway, thereby conferring radiotherapy resistance to colorectal cancer cells. Our study suggests that targeting CNOT7 could serve as a potential therapeutic strategy for rectal cancer patients

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RNA IP Seq analysis of Cnot7 in 4T1 mammary tumor cells

2015-09-23 | E-GEOD-73366 | biostudies-arrayexpress

Effect of Cnot7 expression on 4T1 mammary tumor cell line transcriptome

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Poly(A) tail length profiling of mRNAs from fission yeast

Project description:To obtain global data on polyadenylation of mRNAs, we fractionated the mRNAs according to their poly(A) tail length using a poly-U sepharose column followed by differential elution at five temperatures. Five mRNA fractions with distinct ranges of poly(A) tail length were then hybridized to microarrays using total eluate as a reference.

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hCAF1/CNOT7 regulates interferon signaling by targeting STAT1

Project description:Stringent regulation of the interferon signaling pathway is essential for maintaining the immune response to pathogens and tumors. The transcription factor STAT1 is a crucial mediator of this response. Here we show that hCAF1/CNOT7 regulates class I and II interferon pathways at different crucial steps. In resting cells hCAF1 can control STAT1 trafficking by interacting with the latent form of STAT1 in the cytoplasm. IFN treatment induces STAT1 release, suggesting that hCAF1 may shield cytoplasmic STAT1 from undesirable stimulation. Consistent, hCAF1 silencing enhances STAT1 basal promoter occupancy associated with increased expression of a subset of STAT1-regulated genes. Consequently, hCAF1 knockdown cells exhibit an increased protection against viral infection and reduced viral replication. Furthermore, hCAF1 participates in the extinction of the IFN signal, through its deadenylase activity, by speeding up the degradation of some STAT1-regulated mRNAs. Since abnormal and unbalanced JAK/STAT activation is associated with immune disorders and cancer, hCAF1 could play a major role in innate immunity and oncogenesis, contributing to tumor escape. mRNAs from cells expressing the siRNA siRNA duplexes targeting hCAF1, corresponding to the coding region 941-961 (kd) (hCAF1 NCBI Reference Sequence: NM_013354.5) and one non-targeting control siRNA (mock).

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2015-09-22 | E-GEOD-73296 | biostudies-arrayexpress

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Project description:siRNA-mediated knockdown of CNOT6 and/or CNOT6L, or CNOT7 and CNOT8 compared to control to study role in the regulation of gene expression by these factors.

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