Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Inhibition of DUSP18 impairs cholesterol biosynthesis and promotes anti-tumor immunity in colorectal cancer

ABSTRACT: To explore the role of Dusp18 in regulating the immune microenvironment of colorectal cancer (CRC), we established MC38 knockdown via shRNA and performed the proteomics.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Colon

DISEASE(S): Colon Cancer

SUBMITTER: zhou xiaojun

LAB HEAD: Li youjun

PROVIDER: PXD053284 | Pride | 2024-07-12

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	CT1_1.raw	Raw
	CT1_2.raw	Raw
	CT1_3.raw	Raw
	CT1_4.raw	Raw
	CT2_1.raw	Raw

Items per page:

1 - 5 of 25

Similar Datasets

Raw data of DIA proteome in large and small body Lijiang pigs

Project description:Analyze the raw data of the DIA proteome of the longissimus dorsi muscle of 0-month-old and 6-month-old large and small Lijiang pigs to obtain differential proteins

2024-10-17 | PXD045863 | Pride

Livin is upregulated in keratinocytes and promotes the release of inflammatory mediators in psoriasis

Project description:Psoriasis is a common chronic inflammatory skin disease. Keratinocytes (KCs) are important effector cells that can recruit inflammatory cells by releasing inflammatory factors and chemokines to promote the inflammatory cascade in psoriasis. However, the mechanism underlying KC activation in psoriasis remains unclear. Livin is an inhibitor of apoptotic proteins and its expression can directly affect the proliferation and metastasis of tumor cells. Livin expression has been reported to be significantly increased in the lesions of patients with psoriasis; however, its specific role in KC activation has not yet been reported. The aim of this study was to investigate whether livin regulates KC activation and causes the release of inflammatory mediators. The expression levels of livin in patients with psoriasis, an imiquimod (IMQ) mouse model, and M5-treated HaCaT cells were determined via immunofluorescence staining, reverse transcription-quantitative polymerase chain reaction, enzyme-linked immunosorbent assay (ELISA), and western blotting. We constructed livin knockdown (Knockdown-HaCaT) and negative control (NC-HaCaT) cells using human immunodeficiency virus-1-based lentiviral vectors to study the function of livin in KCs via RNA-sequencing and proteomics analysis. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed. Moreover, the effect of livin expression on the release of inflammatory mediators in KCs was verified using ELISA.

2024-05-22 | PXD035174 | Pride

PLA2G4A promotes right-sided colorectal cancer progression by inducing CD39+γδ Tregs polarization

Project description:Here, we discovered that the frequency of CD39+γδ Tregs, which positively correlated with poor prognosis, was significantly higher in right-sided colorectal cancer (RSCRC) than in the left-sided CRC (LSCRC). To explore the molecular mechanism leading to the difference of CD39+γδ Tregs derived from RSCRC and LSCRC, we collected fresh tissue samples of RSCRC with high expression of CD39+γδ Tregs and the LSCRC with low expression of CD39+γδ Tregs detected by flow cytometry and identified differential proteins by LC-MS based quantitative proteomic analysis with tandem mass tag (TMT)

2022-02-17 | PXD027323 | Pride

Proteomic analysis reveals critical immunomolecular mechanisms in macrophage anti-tuberculosis processes

Project description:Tuberculosis infection activates the autoimmune system. However, the role of autoimmunity after Mycobacterium tuberculosis infection is unclear. In this study, liquid chromatography-tandem mass spectrometry (LC-MS/MS) combined with tandem mass spectrometry (TMT) was used to perform proteomic analysis of five spinal tuberculosis and five protruding disc tissue samples. The identification of key molecular mechanisms provides a molecular target for future treatment of spinal tuberculosis, which may significantly improve patients' quality of life and prognosis.

2021-01-04 | PXD022541 | Pride

LINC00839 promotes malignancy of liver cancer via binding FMNL2 under hypoxia

Project description:Liver cancer is one of the most common malignant tumors in the world and metastasis is the leading cause of death associated with liver cancer. Hypoxia is a common feature of solid tumors and enhances malignant character of cancer cells. However, the exact mechanisms involved in hypoxia-driven liver cancer progression and metastasis have not been well clarified so far. The aim of this study was to investigate the contribution of long non-coding RNA (lncRNA) in hypoxia promoting liver cancer progression. We screened and revealed LINC00839 as a novel hypoxia-responsive lncRNA in liver cancer. LINC00839 expression was up-regulated in liver cancer tissues and cell lines, and the patients with high LINC00839 expression had shortened overall survival. LINC00839 further overexpressed under hypoxia and promoted liver cancer cell proliferation, migration, and invasion. Mechanistically, LINC00839 bound multiple proteins that were primarily associated with the metabolism and RNA transport, and positively regulated the expression of Formin-like protein 2 (FMNL2). LINC00839 could promote hypoxia-mediated liver cancer progression, suggesting it may be a clinically valuable biomarker and serve as a molecular target for the diagnosis, prognosis, and therapy of liver cancer.

2023-03-11 | PXD034526 | Pride

DPAGT1-Mediated Protein N-Glycosylation Is Indispensable for Oocyte and Follicle Development in Mice

Project description:Posttranslational modification of proteins by N-linked glycosylation is crucial for many life processes. However, the exact contribution of N-glycosylation to mammalian female reproduction remains largely undefined. Here, DPAGT1, the enzyme that catalyzes the first step of protein N-glycosyation, is identified to be indispensable for oocyte development in mice. A recessive missense mutation (c. 497A>G; p. Asp166Gly) of Dpagt1 causes female subfertility without grossly affecting other functions. Mutant females ovulate fewer eggs owing to defects of follicular development beyond the late secondary stage. Oocytes ovulated by mutants carry a thin and fragile zona pellucida, and display poor developmental competence after fertilization in vitro. Moreover, completion of the first meiosis is accelerated in mutant oocytes, which is coincident with the elevation of aneuploidy. Mechanistically, transcriptomic analysis reveals the downregulation of a number of transcripts essential for oocyte meiotic progression and preimplantation development (e.g., Pttgt1, Esco2, Orc6, and Npm2) in mutant oocytes, which could account for the defects observed. Furthermore, conditional knockout (CKO) of Dpagt1 in oocytes recapitulates the phenotypes observed in Dpagt1 mutant females, and causes complete infertility. Taken together, these data indicate that protein N-glycosylation in oocytes is essential for female fertility in mammals by specific control of oocyte development.

2021-09-09 | PXD018531 | Pride

Proteomics analysis of HepG2 after administration of dehydroabietic acid

Project description:Proteomics identification of the HepG2 test group after administration of dehydroabietic acid was implemented to disclose the influencing mechanism of dehydroabietic acid on HepG2.

2022-11-22 | PXD036015 | Pride

Comprehensive proteomic analysis of exosome mimetic vesicles and exosomes derived from human umbilical cord mesenchymal stem cells

Project description:Exosomes derived from mesenchymal stem cells (MSCs) have shown to have effective application prospects in the medical field, but exosome yield is very low. The production of exosome mimetic vesicles (EMVs) by continuous cell extrusion leads to more EMVs than exosomes, but whether the protein compositions of MSC-derived EMVs (MSC-EMVs) and exosomes (MSC-exosomes) are substantially different remains unknown. The purpose of this study was to conduct a comprehensive proteomic analysis of MSC-EMVs and MSC-exosomes and to simply explore the effects of exosomes and EMVs on wound healing ability. This study provides a theoretical basis for the application of EMVs and exosomes.In this study, EMVs from human umbilical cord MSCs (hUC MSCs) were isolated by continuous extrusion, and exosomes were identified after hUC MSC ultracentrifugation. A proteomic analysis was performed, and 2,315 proteins were identified. The effects of EMVs and exosomes on the proliferation, migration and angiogenesis of human umbilical vein endothelial cells (HUVECs) were evaluated by cell counting kit-8, scratch wound, Transwell and tubule formation assays. A mouse mode was used to evaluate the effects of EMVs and exosomes on wound healing . Bioinformatics analyses revealed that 1,669 proteins in both hUC MSC-EMVs and hUC MSC-exosomes play roles in retrograde vesicle-mediated transport and vesicle budding from the membrane. The 382 proteins unique to exosomes participate in extracellular matrix organization and extracellular structural organization, and the 264 proteins unique to EMVs target the cell membrane. EMVs and exosomes can promote wound healing and angiogenesis in mice and promote the proliferation, migration and angiogenesis of HUVECs.

2022-08-11 | PXD033899 | Pride

Mass spectrometry (MS) datasets of PURPL RNA pulldown samples in A375 cells

Project description:We performed PURPL RNA pulldown followed by MS analysis to identify purpl-interacting proteins in A375 cells.With high performance liquid chromatography-mass spectrometry (HPLC-MS), the binding protein of PURPL from RNA pull down was detected by removing non-specific protein which were binding with EGFP.

2022-02-16 | PXD028863 | Pride

Coiled-Coil Domain-Containing 68 Downregulation Promotes Colorectal Cancer Cell Growth by Inhibiting ITCH-Mediated CDK4 Degradation

Project description:Coiled-coil domain-containing 68 (CCDC68) plays different roles in cancer and is predicted as a tumor suppressor in human colorectal cancer (CRC). However, the specific role of CCDC68 in CRC and the underlying mechanisms remain unknown. Here, we showed that CCDC68 expression was lower in CRC than in corresponding normal tissues, and CCDC68 level was positively correlated with disease-free survival. Ectopic expression of CCDC68 decreased CRC cell proliferation in vitro and suppressed the growth of CRC xenograft tumors in vivo. CCDC68 caused G0/G1 cell cycle arrest, downregulated CDK4, and upregulated ITCH, the E3 ubiquitin ligase responsible for CDK4 protein degradation. This increased CDK4 degradation, which decreased CDK4 protein levels and inhibited CRC tumor growth. Collectively, the present results identify a novel CDK4 regulatory axis consisting of CCDC68 and ITCH, which suggest that CCDC68 is a promising target for the treatment of CRC.

2021-04-14 | PXD024343 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data