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NXN suppresses metastasis of hepatocellular carcinoma by promoting degradation of Snail through binding to DUB3

ABSTRACT: NXN suppresses metastasis of hepatocellular carcinoma by promoting degradation of Snail through binding to DUB3

PROVIDER: PRJNA860848 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20340271_1.fastq.gz	Fastqsanger.gz
	SRR20340271_2.fastq.gz	Fastqsanger.gz
	SRR20340272_1.fastq.gz	Fastqsanger.gz
	SRR20340272_2.fastq.gz	Fastqsanger.gz
	SRR20340273_1.fastq.gz	Fastqsanger.gz

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NXN suppresses metastasis of hepatocellular carcinoma by promoting degradation of Snail through binding to DUB3

Project description:To investigate the function of NXN in the regulation of metastasis in hepatocellular carcinoma cells, we established NXN knock down Hep-3B cells by shRNA. We then performed gene expression profiling analysis using data obtained from RNA-seq of 2 different cells at three time points.

2022-07-26 | GSE208734 | GEO

NXN suppresses metastasis of hepatocellular carcinoma by promoting degradation of Snail through binding to DUB3.

Project description:The poor prognosis of hepatocellular carcinoma (HCC) could be attributed to its high metastasis rate. Here, we report the role of nucleoredoxin (NXN), a multifunctional redox-active protein, in HCC metastasis. The expression of NXN in HCC tissues was measured by immunohistochemistry. The role of NXN on HCC proliferation was determined by CCK-8, EdU and colony formation assays in vitro and subcutaneous tumor formation model in vivo. Transwell and wound healing assays and tail vein injection model were performed to assess the function of NXN on HCC metastasis. Co-immunoprecipitation assay was performed to examine the interaction among NXN, Snail and DUB3. Our results showed that NXN was downregulated in HCC tissues compared to adjacent liver tissues. Patients with low NXN expression had shorter overall survival (OS) time (P < 0.001) than those with high NXN expression. Biologically, ectopic expression of NXN significantly inhibited the proliferation and metastasis of HCC cells both in vitro and in vivo by suppressing epithelial-mesenchymal transition (EMT). Mechanistically, NXN promoted the ubiquitin-proteasome-mediated degradation of Snail through interaction with DUB3. Further, depletion of Snail abolished NXN-inhibited cell proliferation and metastasis. In summary, NXN suppressed the proliferation and metastasis of HCC by inhibiting DUB3-mediated deubiquitylation of Snail protein. Our study demonstrates that NXN, DUB3 and Snail complex functioned as an important regulatory mechanism of HCC progression and indicates a potential therapeutic approach for the treatment of HCC metastasis.

| S-EPMC9352874 | biostudies-literature

GINS4 suppresses ferroptosis by antagonizing p53 acetylation with Snail

Project description:GINS4 suppresses ferroptosis by antagonizing p53 acetylation with Snail.

2023-03-21 | PXD040993 |

Omeprazole suppresses aggressive cancer growth and metastasis in mice through promoting Snail degradation.

Project description:Omeprazole is a proton pump inhibitor that has recently been reported to exhibit anticancer activity against several types of cancer. However, the anticancer mechanisms of omeprazole remain elusive. Snail is an oncogenic zinc finger transcription factor; aberrant activation of Snail is associated with the occurrence and progression of cancer. In this study, we investigated whether Snail acted as a direct anticancer target of omeprazole. We showed that omeprazole displayed a high binding-affinity to recombinant Snail protein (Kd = 0.076 mM), suggesting that omeprazole directly and physically binds to the Snail protein. We further revealed that omeprazole disrupted CREB-binding protein (CBP)/p300-mediated Snail acetylation and then promoted Snail degradation through the ubiquitin-proteasome pathway in HCT116 cells. Omeprazole treatment markedly suppressed Snail-driven epithelial-mesenchymal transition (EMT) in aggressive HCT116, SUM159, and 4T1 cancer cells in vitro and reduced EMT-associated tumor invasion and metastasis in cancer cell xenograft models. Omeprazole also inhibited tumor growth by limiting Snail-dependent cell cycle progression. Overall, this study, for the first time, identifies Snail as a target of omeprazole and reveals a novel mechanism underlying the therapeutic effects of omeprazole against cancer. This study strongly suggests that omeprazole may be an excellent auxiliary drug for treating patients with malignant tumors.

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Galectin-9 suppresses growth of hepatocellular carcinoma in vitro

Project description:Galectin-9 suppresses growth of Li-7 cells, a cell line of human hepatocellular carcinoma, in vitro study. Micro RNA expression of Li-7 cells, a cell line of hepatocellular carcinoma, with or without administration of galectin-9 were assessed in vitro.

2015-03-01 | E-GEOD-55665 | biostudies-arrayexpress

Galectin-9 suppresses growth of hepatocellular carcinoma in vivo

Project description:Galectin-9 suppresses growth of Li-7 cells, a cell line of human hepatocellular carcinoma, in xenograft model analysis. Micro RNA expression in xenografts of Li-7 cells, a cell line of hepatocellular carcinoma, with or without administration of galectin-9 were assessed.

2015-03-01 | E-GEOD-55666 | biostudies-arrayexpress

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

Galectin-9 suppresses growth of hepatocellular carcinoma in vitro

Project description:Galectin-9 suppresses growth of Li-7 cells, a cell line of human hepatocellular carcinoma, in vitro study.

2015-03-01 | GSE55665 | GEO

Galectin-9 suppresses growth of hepatocellular carcinoma in vivo

Project description:Galectin-9 suppresses growth of Li-7 cells, a cell line of human hepatocellular carcinoma, in xenograft model analysis.

2015-03-01 | GSE55666 | GEO

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

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

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