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The UNC5D-NuRD Repressor Complex Promotes Breast Cancer Progression by Negatively Regulating GSK3B

ABSTRACT: The UNC5D-NuRD Repressor Complex Promotes Breast Cancer Progression by Negatively Regulating GSK3B

PROVIDER: PRJNA1124014 | ENA |

REPOSITORIES: ENA

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			Action	DRS
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	SRR29411983_1.fastq.gz	Fastqsanger.gz
	SRR29411983_2.fastq.gz	Fastqsanger.gz

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The UNC5D-NuRD Repressor Complex Promotes Breast Cancer Progression by Negatively Regulating GSK3B

Project description:Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for UNC5D in MDA-MB-231 cells. UNC5D serves as a receptor for Netrin-1 and is highly expressed in breast cancer. Here, we report that UnICD, generated by caspase cleavage of UNC5D, translocates to the nucleus, interacts with the NuRD complex, and promotes tumorigenesis and development by relieving or reducing its suppression of β-catenin through inhibiting the transcription of GSK3B. In vitro experiments showed that the knockdown of UNC5D can inhibit the proliferation of breast cancer cells. Consistently, the expression level of UNC5D in breast cancer was negatively correlated with the expression level of GSK3B, and high levels of UNC5D were associated with poor prognosis in breast cancer patients. These results suggest that UNC5D is a pivotal driver in breast carcinogenesis, potentially inducing the initiation and progression of breast cancer through the UnICD/NuRD-GSK3B-β-catenin axis.

2025-06-14 | GSE269850 | GEO

Co-repressor CDYL confers forebrain identity to human cortical organoids by negatively regulating NNAT

Project description:Co-repressor CDYL confers forebrain identity to human cortical organoids by negatively regulating NNAT

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The CXXC5-CRL4B-NuRD Repressor Complex Promotes Breast Carcinogenesis by Regulating the TSC1/mTOR pathway

Project description:The CXXC5-CRL4B-NuRD Repressor Complex Promotes Breast Carcinogenesis by Regulating the TSC1/mTOR pathway

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Co-repressor CDYL confers forebrain identity to human cortical organoids by negatively regulating NNAT [RNA-Seq]

Project description:Co-repressor CDYL confers forebrain identity to human cortical organoids by negatively regulating NNAT [RNA-Seq]

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Co-repressor CDYL confers forebrain identity to human cortical organoids by negatively regulating NNAT [ChIP-Seq]

Project description:Co-repressor CDYL confers forebrain identity to human cortical organoids by negatively regulating NNAT [ChIP-Seq]

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JA-INDUCIBLE MYC2-LIKE1 acts as a repressor and negatively regulates jasmonate signaling in Arabidopsis

Project description:Jasmonate (JA) is a plant hormone that controls trade-offs between plant growth and responses to biotic and abiotic stresses. Although recent studies uncover core mechanism for JA-induced responses in Arabidopsis thaliana, it remains elusive how plants attenuate those responses. We report here that a basic-helix-loop-helix type transcription factor named JA-INDUCIBLE MYC2-LIKE1 (JAM1) acts as a transcriptional repressor and negatively regulates JA signaling. Arabidopsis plants expressing the chimeric repressor for JAM1 exhibited a substantial reduction of JA responses, including JA-induced inhibition of root growth, accumulation of anthocyanin, and male fertility. These plants were also compromised in resistance to attack by Spodoptera exigua. Conversely, jam1-4 loss-of-function mutants showed enhanced JA responsiveness, including increased resistance to the insect attack. Competitive binding of JAM1 and MYC2 to the target sequence of MYC2 suggested negative regulation of JA signaling by JAM1 and suppression of MYC2 function. These results indicate that JAM1 plays a pivotal role in fine-tuning of JA-mediated stress responses and plant growth by negatively regulating JA signaling. Transcriptomes of ProJAM1:JAM1-SRDX, ProMYC2:MYC2-SRDX and wild-type Arabidopsis seedlings with or without jasmonic acid were compared.

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The CXXC5-CRL4B-NuRD Repressor Complex Promotes Breast Carcinogenesis by Regulating the TSC1/mTOR pathway

Project description:Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for CXXC5,CUL4B as well as MTA1 in MCF-7 cells.The pathophysiological function of the CXXC family-member CXXC5 remains to be explored. Here we report that CXXC5 is physically associated with the CRL4B complex and the NuRD complex. Genome-wide investigation of transcriptional targets revealed that the CXXC5/CRL4B/NuRD complex represses a panel of genes including TSC1 that are critically involved in cell growth and the regulation of the mTOR pathway, leading to activation of PD-L1. Intriguingly, CXXC5 expression was increased after stimulation with vitamin B2, whereas vitamin D treatment was accompanied by decreased expression of CXXC5. We demonstrated that the CXXC5-CRL4B-NuRD complex promotes cancer cell proliferation. Elevation of CXXC5, CUL4B, and MTA1 expression during cancer progression corresponded to diminished TSC1 expression, and high levels of CXXC5, CUL4B, and MTA1 strongly correlated with higher histological grades and poor prognosis. We further identified that CXXC5 is bimodally regulated by different kinds of vitamins. Our study revealed that CXXC5-mediated TSC1 suppression activates the mTOR pathway, reduces autophagic cell death, induces PD-L1-mediated immune suppression and results in tumor development, providing a possible mechanistic insight into the pathophysiological function of CXXC5.

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JA-INDUCIBLE MYC2-LIKE1 acts as a repressor and negatively regulates jasmonate signaling in Arabidopsis

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GSK3B shRNA in Panc-1 xenografts

Project description:The Panc-1 human pancreatic cancer line (ATCC) was constructed to stably express control or GSK3B shRNA. Control or GSK3B shRNA expressing Panc-1 cells were implanted subcutaneously into the flanks of 3-5 week old, female, athymic nude mice. Tumors were grown to at least 250mm3. Tumor tissue was microdissected for further analysis. We compared control shRNA (n=4) to GSK3B shRNA (n=3) Panc-1 xenografts. The array data with simple statistical calculations are also provided in a supplementary Excel workbook, with probe-set annotation that we used at the time (users may want newer annotation). We compared xenografts of Panc-1 (Human pancreatic carcinoma cell line, grown in mice) stably expressing GSK3B shRNA (n=3) to similar xenografts with control shRNA (n=4). Xenografts were grown in the flanks of female, athymic nude mice until they reached at least 250mm3. Tumor tissue was microdissected for further analysis. mRNA abundance assays were performed using Affymetrix HG_U133_plus_2 arrays, with 54675 probe-sets.

2014-01-09 | E-GEOD-35351 | biostudies-arrayexpress

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