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Human hepatocellular carcinoma Orbitrap-LC-MS-HZ

ABSTRACT: Human hepatocellular carcinoma cells were subcutaneously implanted into nude mice and treated with photodynamic nanoparticles (NP3) with laser, followed by tissue collection and proteomic analysis.

INSTRUMENT(S): LTQ Orbitrap

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Liver

SUBMITTER: Huiling Zhou

LAB HEAD: Haihua Xiao

PROVIDER: PXD041112 | Pride | 2023-10-24

REPOSITORIES: Pride

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			Action	DRS
	Human-HCC-LC-MS-HZ-File2.mzTab	Mztab
	MS1.raw	Raw
	MS10.raw	Raw
	MS11.raw	Raw
	MS12.raw	Raw

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1 - 5 of 14

Publications

Theranostic imaging and multimodal photodynamic therapy and immunotherapy using the mTOR signaling pathway.

Zhou Huiling H Tang Dongsheng D Yu Yingjie Y Zhang Lingpu L Wang Bin B Karges Johannes J Xiao Haihua H

Nature communications 20230902 1

Tumor metastases are considered the leading cause of cancer-associated deaths. While clinically applied drugs have demonstrated to efficiently remove the primary tumor, metastases remain poorly accessible. To overcome this limitation, herein, the development of a theranostic nanomaterial by incorporating a chromophore for imaging and a photosensitizer for treatment of metastatic tumor sites is presented. The mechanism of action reveals that the nanoparticles are able to intervene by local genera ...[more]

PMID: 37660174

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Transcription profiling of human A549 induced tumours in mice treated with PCI-5002, PCI-5003, or control vehicle

Project description:We have demonstrated that water-soluble zinc ionophores can be administered to mice at relatively high doses and inhibit the growth of A549 lung cancer cells grown in xenograft models. Gene expression profiles of tumor specimens harvested from mice four hours after treatment confirmed that the activation of stress responsive genes occurs in vivo. These findings lead us to propose that the pharmacologic delivery of zinc to tumors using water solubilized ionophores is a potential approach to cancer therapy. Experiment Overall Design: 1.25 million A549 cells were injected subcutaneously/intramuscularly into the right hind flank of 6 week old CD-1 nude mice that had been irradiated with 4 Gy of total body irradiation from a 137Cs radiation source one day prior to tumor implantation. When the average size of tumors reached approximately 100 mm3, mice were randomized by tumor size to treatment groups, typically containing 6-8 mice per group. Tumor and body weight measurements were performed three times per week. Tumor volume was calculated using the equation V (mm3) = a x b2/2, where a is the largest diameter and b is the smallest diameter. No significant body weight loss was observed. To perform gene expression profiling, mice were treated intravenously with one dose (100 Î¼mol/kg) PCI-5002, PCI-5003, or control vehicle (4 mice per group) when the average A549 tumor size reached 500 mm3. After four hours, tumors were harvested and snap frozen immediately on dry ice. Tumor tissue was homogenized, and total RNA was isolated and subjected to analysis using Human Genome U133 Plus 2.0 Arrays as described above.

2008-06-15 | E-GEOD-6962 | biostudies-arrayexpress

Ischemic stroke mice brain LC-MSMS

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2024-08-02 | PXD049258 | Pride

Nogo-B co-IP-MS experiment in mouse liver and pancreas

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NOD Mouse Islet Peptide Content Identification

Project description:Beta-cells produce hybrid insulin peptides (HIPs) by linking insulin fragments to other peptides through peptide bonds. HIPs have unique amino acid sequences and are targeted by autoreactive T cells in type 1 diabetes (T1D). Individuals with recent-onset T1D have significantly higher levels of HIP-reactive T cells in their blood compared to non-diabetic control subjects. HIP-reactive T cells have also been found in the residual pancreatic islets of deceased T1D organ donors. In non-obese diabetic (NOD) mice, a major T1D animal model, several CD4 T cell clones that trigger diabetes have been shown to target HIPs. Through mass spectrometry, a subgroup of HIPs containing N-terminal amine groups of various peptides linked to aspartic acid residues of insulin C-peptide has been detected in NOD islets. Our research reveals that these HIPs form spontaneously in beta-cells via an aspartic anhydride intermediate mechanism. This process leads to the creation of a regular HIP with a standard peptide bond and a HIP-isomer (isoHIP) with an isopeptide bond linked to the carboxylic acid side-chain of the aspartic acid residue. Our mass spectrometric analyses confirmed the presence of both HIP isomers in murine islets, thereby validating the occurrence of this new reaction mechanism in beta-cells. The spontaneous formation of neoepitopes through the development of new peptide bonds within cells may contribute to the pathogenesis of T1D and other autoimmune diseases.

2023-11-16 | PXD041616 | Pride

Quantitative analysis of proteome dynamics in a long-term asthma mouse model

Project description:Asthma bronchiale is an inflammatory disease of the respiratory airways and a major factor of increasing health care costs worldwide. The molecular actors leading to asthma are not fully understood and require further investigation. The aim of this study was to monitor the proteome during asthma development from early inflammatory to late fibrotic stages. A time-course-based ovalbumin (OVA) mouse model was applied to establish an asthma phenotype and the lung proteome was analysed at four time points during asthma development (0 weeks = control, 5 weeks, 8 weeks and 12 weeks of OVA treatment).

2021-02-11 | PXD011159 | Pride

A549 treated with CISPLATIN/TSA VS CONTROL

Project description:WE TEST THE PROTEIN CHANGES WHEN A549 cells treated with DDP OR TSA.

2024-06-23 | PXD052305 | Pride

A549 cell treated with DDP+TSA vs DDP

Project description:analysis how HDAC inhibitior TSA increase cispkatin cytotoxicity

2024-06-23 | PXD052203 | Pride

RNA-seq analysis of normoxic and hypoxic tumor-associated macrophages

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2018-01-01 | E-MTAB-5032 | biostudies-arrayexpress

Integrated phosphoproteome, ubiquitinome, and acetylome analyses uncovering the post-translational modifications crosstalk during MSP1-induced signaling in rice

Project description:Magnaporthe oryzae snodprot1 homologous protein (MSP1) has been shown to act as a pathogen-associated molecular pattern (PAMPs) and trigger PAMP-triggered immunity (PTI) response involving programmed cell death and expression of various defense-related genes in rice. The involvement of several post-translational modifications (PTMs) in the regulation of plant immune response, especially PTI, during pathogen infection is well established, however, the information on the regulatory roles of these PTMs in response to MSP1-induced signaling in rice is currently elusive. Here, we report the phosphoproteome, ubiquitinome, and acetylproteome to investigate the MSP1-induced PTMs alterations in MSP1 overexpressed rice. Our analysis identified a total of 4,666 PTM modified sites in rice leaves including 4,292 phosphosites, 189 ubiquitin sites, and 185 acetylation sites. Among these, PTM status of 437 phosphorylated, 53 ubiquitinated, and 68 acetylated peptides were significantly changed by MSP1. Functional annotation of MSP1 modulated peptides by MapMan analysis revealed that these were majorly associated with cellular immune responses such as signaling, transcription factors, DNA and RNA regulation, and protein metabolism, among others. Taken together, this study uncovers the MSP1-induced PTMs changes in rice proteins and identified several novel components of rice-MSP1 interaction.

2023-07-21 | PXD039997 | Pride

Adaption of oxidative phosphorylation machinery compensates hepatic lipotoxicity in early stages of MAFLD; PMID:35743314

Project description:Mitochondrial function is an important control variable in the progression of metabolic dysfunction associated fatty liver disease (MAFLD). We hypothesize that organization and function of mitochondrial electron transport chain (ETC) in this pathologic condition is a consequence of shifted substrate availability. Paradoxically, in MAFLD increased de novo lipogenesis (DNL) occurs despite hepatic insulin resistance. Therefore, we addressed this question using our animal model alb-SREBP-1c, which exhibits increased DNL by constitutively active SREBP-1c. Using an omics approach, we show that the abundance of ETC complex subunits and metabolic pathways are altered in liver of these animals. Analyses of cellular metabolic status by functional assays revealed that SREBP-1c-forced DNL induces a limitation of substrates for oxidative phosphorylation that is rescued by enhanced complex II activity. Furthermore, energy metabolism associated gene regulation indicates the counteracting to increase expression of mitochondrial genes and features cell communication by miRNA and exosomal RNA transfer. In conclusion, substrate availability fuels mainly complex II electron flows as a consequence of activated DNL with impact on whole body by liver-specific exosomal RNAs in early stages of MAFLD.https://pubmed.ncbi.nlm.nih.gov/35743314/

2022-08-02 | PXD032214 | Pride

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