Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Targeted Ubiquitination and Degradation of GOLM1 by CC-885 Suppresses Hepatocellular Carcinoma Growth and Metastasis

ABSTRACT: Targeted Ubiquitination and Degradation of GOLM1 by CC-885 Suppresses Hepatocellular Carcinoma Growth and Metastasis

PROVIDER: PRJNA1137341 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR29880415_1.fastq.gz	Fastqsanger.gz
	SRR29880415_2.fastq.gz	Fastqsanger.gz
	SRR29880416_1.fastq.gz	Fastqsanger.gz
	SRR29880416_2.fastq.gz	Fastqsanger.gz
	SRR29880417_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Targeted Ubiquitination and Degradation of GOLM1 by CC-885 Suppresses Hepatocellular Carcinoma Growth and Metastasis

Project description:Hepatocellular carcinoma (HCC) is a leading cause of cancer mortality, necessitating innovative therapeutic approaches. This study demonstrates that the compound CC-885 exerts potent anti-tumor effects in HCC both in vitro and in vivo. CC-885 significantly inhibited proliferation, migration, and invasion of HCC cells. In vivo, CC-885 markedly reduced tumor growth and angiogenesis in chick embryo and mouse xenograft models. Mechanistically, CC-885 selectively reduced GOLM1 protein levels via ubiquitin-mediated proteasomal degradation, without affecting its mRNA levels. GOLM1 knockdown mimicked the anti-proliferative effects of CC-885, while overexpression of GOLM1 conferred resistance to CC-885-induced apoptosis and growth inhibition. CC-885 facilitated the interaction between GOLM1 and the E3 ubiquitin ligase CRBN, promoting GOLM1 ubiquitination and degradation. Transcriptomic analyses revealed that CC-885 and GOLM1 knockdown modulated key pathways involved in apoptosis, NF-κB signaling, and cell proliferation. These findings highlight CC-885 as a promising therapeutic agent for HCC, primarily by facilitating the CRBN-dependent degradation of GOLM1, underscoring its potential for clinical application.

2024-10-11 | GSE272556 | GEO

The novel cereblon modulator CC-885 inhibits mitophagy via selective degradation of BNIP3L

Project description:Here, by state-of-the-art mass spectrometry-based quantitative proteomic technology, we systematically screened the potential neo-substrates of a novel thalidomide derived cereblon modulator CC-885.

2020-01-11 | PXD017071 |

Gene expression of keratinocytes with miR-885-5p inhibited vs control

Project description:As miR-885-5p is a microRNA downregulated in Cutaneous Lupus Erythematosus (CLE) and it is localted in the epidemis and its function is focused in keratinocytes, human Arrays to study the role of miR-885-5p in Cutaneous Lupus Erythematosius will be conducted.Gene expression in keratinocytes transfected with anti-miR-885-5p will be studied. We have included 24 Samples: Non-stimulated control (4), Non-stimulated anti-miR-885-5p (4), UVB-stimulated control (4), UVB-stimulated antimiR-885-5p (4), IFN alpha-stimulated control (4) and IFN alpha-stimulated anti-miR-885-5p

2022-07-19 | GSE193090 | GEO

A Novel Cereblon Modulator Targets eRF3 Family Proteins For Cereblon-dependent Destruction

Project description:To discern why GSPT1 depletion induced growth inhibition, we utilized RNA microarray analysis to profile the transcriptional changes in cells treated with CC-885 or DMSO. To discern why CC-885 induced growth inhibition, we utilized RNA microarray analysis to profile the transcriptional changes in cells treated with CC-885 or DMSO Several key markers of the ATF4 pathway including ATF3, CHOP (DDIT3), and ATF4 were significantly induced by CC-885 treatment.

2018-12-17 | GSE76195 | GEO

The novel cereblon modulator CC-885 inhibits mitophagy via selective degradation of BNIP3L.

Project description:Mitophagy is a degradative pathway that mediates the degradation of the entire mitochondria, and defects in this process are implicated in many diseases including cancer. In mammals, mitophagy is mediated by BNIP3L (also known as NIX) that is a dual regulator of mitochondrial turnover and programmed cell death pathways. Acute myeloid leukemia (AML) cells with deficiency of BNIP3L are more sensitive to mitochondria-targeting drugs. But small molecular inhibitors for BNIP3L are currently not available. Some immunomodulatory drugs (IMiDs) have been proved by FDA for hematologic malignancies, however, the underlining molecular mechanisms are still elusive, which hindered the applications of BNIP3L inhibition for AML treatment. In this study we carried out MS-based quantitative proteomics analysis to identify the potential neosubstrates of a novel thalidomide derivative CC-885 in A549 cells. In total, we quantified 5029 proteins with 36 downregulated in CRBN+/+ cell after CC-885 administration. Bioinformatic analysis showed that macromitophagy pathway was enriched in the negative pathway after CC-885 treatment. We further found that CC-885 caused both dose- and time-dependent degradation of BNIP3L in CRBN+/+, but not CRBN-/- cell. Thus, our data uncover a novel role of CC-885 in the regulation of mitophagy by targeting BNIP3L for CRL4CRBN E3 ligase-dependent ubiquitination and degradation, suggesting that CC-885 could be used as a selective BNIP3L degradator for the further investigation. Furthermore, we demonstrated that CC-885 could enhance AML cell sensitivity to the mitochondria-targeting drug rotenone, suggesting that combining CC-885 and mitochondria-targeting drugs may be a therapeutic strategy for AML patients.

| S-EPMC7608331 | biostudies-literature

Prevotella sp. 885

Project description:Prevotella sp. 885 Genome sequencing and assembly

| PRJNA395537 | ENA

MTSS1 Suppresses Expansion and Activity of Mammary Tumor-initiating Cells by Mediating P65 Ubiquitination and Degradation

Project description:MTSS1 Suppresses Expansion and Activity of Mammary Tumor-initiating Cells by Mediating P65 Ubiquitination and Degradation

| PRJNA522687 | ENA

Streptomyces avidinii strain:CG 885

Project description:Kitasatospora papulosa CG 885 genome sequencing

| PRJNA330489 | ENA

Populus trichocarpa strain:Besc-885

Project description:Populus trichocarpa strain:Besc-885 Genome sequencing