Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Identification of ubiquitinated proteins in lung adenocarcinoma and normal lung tissues

ABSTRACT: To identify ubiquitinated modified proteins of lung adenocarcinoma, we collected five pairs of lung adenocarcinoma and normal lung tissues from the clinic for analysis

INSTRUMENT(S): timsTOF Pro

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Lung

DISEASE(S): Lung Adenocarcinoma

SUBMITTER: Xu Ran

LAB HEAD: Zhang linyou

PROVIDER: PXD027001 | Pride | 2022-01-12

REPOSITORIES: pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	Ubiquitylome.zip	Other
	Ubiquitylome_cancer_13_Slot2-24_1_9953.d.zip	Other
	Ubiquitylome_cancer_16_Slot2-25_1_9955.d.zip	Other
	Ubiquitylome_cancer_3_Slot2-21_1_9947.d.zip	Other
	Ubiquitylome_cancer_7_Slot2-22_1_9949.d.zip	Other

Items per page:

1 - 5 of 11

Publications

Identification of ubiquitinated substrate proteins and their gene expression patterns in lung adenocarcinoma.

Xu Ran R Lu Tong T Zhao Jiaying J Li Qi Q Wang Jun J Peng Bo B Liu Jian J Zhang Pengfei P Qu Lidong L Chang Xiaoyan X Yao Lingqi L Zhang Linyou L

Annals of translational medicine 20211101 22

<h4>Background</h4>Lung cancer is a malignant disease with the highest cancer-related mortality rate. In lung adenocarcinoma (LUAD), protein ubiquitination can regulate multiple biological processes. A LUAD ubiquitylome analysis has not yet been reported.<h4>Methods</h4>We used for the first time ion mobility into liquid chromatography-mass spectrometry to perform accurate and reliable ubiquitylome and proteomic analysis of clinical LUAD and normal tissues and combined it with transcriptome data ...[more]

PMID: 34988201

Similar Datasets

Proteomic Identification of Lung Adenocarcinoma and Normal Lung Tissue

Project description:To identify proteomic of lung adenocarcinoma, we collected five pairs of lung adenocarcinoma and normal lung tissues from the clinic for analysis

2022-01-12 | PXD027008 | Pride

Ito2019 - gefitnib resistance of lung adenocarcinoma caused by MET amplification

Project description:The model is based on publication: Mathematical analysis of gefitinib resistance of lung adenocarcinoma caused by MET amplification Abstract: Gefitinib, one of the tyrosine kinase inhibitors of epidermal growth factor receptor (EGFR), is effective for treating lung adenocarcinoma harboring EGFR mutation; but later, most cases acquire a resistance to gefitinib. One of the mechanisms conferring gefitinib resistance to lung adenocarcinoma is the amplification of the MET gene, which is observed in 5–22% of gefitinib-resistant tumors. A previous study suggested that MET amplification could cause gefitinib resistance by driving ErbB3-dependent activation of the PI3K pathway. In this study, we built a mathematical model of gefitinib resistance caused by MET amplification using lung adenocarcinoma HCC827-GR (gefitinib resistant) cells. The molecular reactions involved in gefitinib resistance consisted of dimerization and phosphorylation of three molecules, EGFR, ErbB3, and MET were described by a series of ordinary differential equations. To perform a computer simulation, we quantified each molecule on the cell surface using flow cytometry and estimated unknown parameters by dimensional analysis. Our simulation showed that the number of active ErbB3 molecules is around a hundred-fold smaller than that of active MET molecules. Limited contribution of ErbB3 in gefitinib resistance by MET amplification is also demonstrated using HCC827-GR cells in culture experiments. Our mathematical model provides a quantitative understanding of the molecular reactions underlying drug resistance.

2024-09-02 | BIOMD0000000827 | BioModels

Characterizing the secretome of EGFR mutant lung adenocarcinoma

Project description:Lung cancer is the leading cause of cancer related death worldwide, mainly due to the late stage of disease at the time of diagnosis. Non-invasive biomarkers are needed to supplement existing screening methods to enable earlier detection and increased patient survival. This is critical to EGFR-driven lung adenocarcinoma as it commonly occurs in individuals who have never smoked and do not qualify for current screening protocols. Methods: In this study, we performed mass spectrometry analysis of the secretome of cultured lung cells representing different stages of mutant EGFR driven transformation, from normal to fully malignant. Identified secreted proteins specific to the malignant state were validated using orthogonal methods and their clinical activity assessed in lung adenocarcinoma patient cohorts. Results: We quantified 1020 secreted proteins, which were compared for differential expression between stages of transformation. We validated differentially expressed proteins at the transcriptional level in clinical tumor specimens, association with patient survival, and absolute concentration to yield three biomarker candidates: MDK, GDF15, and SPINT2. These candidates were validated using ELISA and increased levels were associated with poor patient survival specifically in EGFR mutant lung adenocarcinoma patients. Conclusions: Our study provides insight into changes in secreted proteins during EGFR driven lung adenocarcinoma transformation that may play a role in the processes that promote tumor progression. The specific candidates identified can harnessed for biomarker use to identify high risk individuals for early detection screening programs and disease management for this molecular subgroup of lung adenocarcinoma patients.

2024-01-03 | PXD045328 | Pride

PARP4 interacts with hnRNPM to regulate splicing during lung cancer progression

Project description:Background: The identification of cancer driver genes from sequencing data has been crucial in deepening our understanding of tumor biology and expanding targeted therapy options. However, apart from the most commonly altered genes, the mechanisms underlying the contribution of other mutations to cancer acquisition remain understudied. Leveraging on our whole-exome sequencing of the largest Asian lung adenocarcinoma (LUAD) cohort (n=302), we now functionally assess the mechanistic role of a novel driver, PARP4. Methods: In vitro and in vivo tumorigenicity assays were used to study the functional effects of PARP4 loss and mutation in multiple lung cancer cell lines. Interactomics analysis by quantitative mass spectrometry was conducted to identify PARP4’s interaction partners. Transcriptomic data from cell lines and patient tumors were used to investigate splicing alterations. Results: PARP4 depletion or mutation (I1039T) promotes the tumorigenicity of KRAS- or EGFR-driven lung cancer cells. Disruption of the vault complex, with which PARP4 is commonly associated, did not alter tumorigenicity, indicating that PARP4’s tumor suppressive activity is mediated independently. The splicing regulator hnRNPM is a potentially novel PARP4 interaction partner, the loss of which likewise promotes tumor formation. hnRNPM loss results in splicing perturbations, with a propensity for dysregulated intronic splicing that was similarly observed in PARP4 knockdown cells and in LUAD cohort patients with PARP4 copy number loss. Conclusions: PARP4 is a novel modulator of lung adenocarcinoma, where its tumor suppressive activity is mediated not through the vault complex – unlike conventionally thought, but in association with its novel interaction partner hnRNPM, thus suggesting a role for splicing dysregulation in LUAD tumorigenesis.

2024-04-02 | PXD050844 | Pride

ChIP-seq of H3K27ac in lung cancer and endometrial carcinoma cells

Project description:Using H3K27ac ChIP-seq profile to map active enhancers in lung cancer and endometrial carcinoma cells ChIP-seq of H3K27ac was done in lung adenocarcinoma cell lines (NCI-H358 and NCI-H2009), squamous cell lung carcinoma cell lines (HCC95) and endometrial carcinoma cell lines (Ishikawa)

2015-10-26 | E-GEOD-66992 | biostudies-arrayexpress

Quantitative tissue proteomics analysis of primary lung adenocarcinoma

Project description:In this study, we generated a quantitative lung tissue proteome dataset from lung adenocarcinoma and adjacent normal lung tissues by using iTRAQ labeling combined with 2D-LC-MS/MS. Based on pathway and network analyses, protein expression profiles released in the public Human Protein Atlas database, literature search and novelty, six candidates were selected for validation via immunohistochemistry staining and western blot. Additionally, the clinical and biological significance of two novel candidates, ERO1L and NARS, was further analyzed. Collectively, our results provide a useful biomarker dataset for lung adenocarcinoma diagnosis/prognosis and provide new insights into ERO1L- and NARS- mediated tumorigenesis.

2022-03-05 | PXD004049 | Pride

Quantitative tissue proteomics analysis of primary lung adenocarcinoma

2016-05-12 | PXD004077 | Pride

Exploring the molecular mechanisms behind the potentiation of chemotherapy effects by durvalumab in lung adenocarcinoma cell lines

Project description:Immune checkpoint inhibitors are increasingly used in combination with chemotherapy for treatment of non-small cell lung cancer, yet the success of combination therapies is relatively limited. Thus, more detailed insight regarding the tumour molecular markers that may affect the responsiveness of patients to therapy is required. Here, we set out to explore the proteome of two lung adenocarcinoma cell lines (HCC-44 and A549) treated with cisplatin, pemetrexed, durvalumab, and the corresponding mixtures to establish the differences in post-treatment protein expression that can serve as markers of chemosensitivity or resistance.

2023-05-12 | PXD040761 | Pride

ZSWIM1 promotes the proliferation and metastasis of lung adenocarcinoma cells through the STK38/MEKK2/ERK1/2 axis

Project description:Investigating the functions of the proteins with no or less functional annotations is an important goal of C-HPP (Chromosome-centric Human Proteome Project). In this study, we investigated the function of such a protein, ZSWIM1 (C20orf162). Its expression is upregulated in lung adenocarcinoma compared with the adjacent normal tissues and negatively correlated with the overall survival (OS). Overexpressing ZSWIM1 markedly promotes the proliferation, migration, invasion as well as epithelial-mesenchymal transition (EMT) in lung adenocarcinoma cells, while knocking down ZSWIM1 functions oppositely. Immunoprecipitation-mass spectrometry (IP-MS) identified the interactome of ZSWIM1 and we verified the interaction of it with the top partner, STK38. ZSWIM1 antagonized the function of STK38. Mechanically, ZSWIM1 promoted the activation of MEKK2/ERK1/2 pathway through interacting with STK38, leading to the release of MEKK2. Taken together, ZSWIM1 can be annotated as an oncogene in lung adenocarcinoma, and the STK38/MEKK2/ERK1/2 axis mediates its promoting role on lung adenocarcinoma.

2023-01-04 | PXD035006 | Pride

LPA MPA SPA lung adenocarcinomas

Project description:Proteomic analysis was performed for three subtypes of lung adenocarcinoma tissues.

2022-10-31 | PXD037831 | JPOST Repository