Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Quantitative proteomics of MYDGF knockdown in lung adenocarcinoma cells

ABSTRACT: Lung adenocarcinoma (LUAD) remains the leading cause of cancer-related mortality worldwide. Unlike patients harboring epidermal growth factor receptor (EGFR) mutations, those with wild-type EGFR lack effective targeted therapeutic options. We established a super-SILAC-based proteomic dataset (PXD046807) comprising LUAD tissues stratified by EGFR mutation status and clinical stages. Notably, myeloid-derived growth factor (MYDGF) was identified as a potential key regulator in patients with wild-type EGFR LUAD. To further investigate the role of MYDGF in LUAD, we applied gene knockdown combined with tandem mass tag (TMT)-based quantitative proteomic analysis to search for the specific biological processes regulated by MYDGF in normal lung fibroblasts and LUAD cells with different EGFR status.

INSTRUMENT(S): Orbitrap Fusion Lumos

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Chia-Jung Yu

LAB HEAD: Chia-Jung Yu

PROVIDER: PXD064751 | Pride | 2025-06-22

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	20220831_CJY_MYDGF_KD_TMT6.msf	Msf
	MYDGF_KD_TMT6_s01.raw	Raw
	MYDGF_KD_TMT6_s02.raw	Raw
	MYDGF_KD_TMT6_s03.raw	Raw
	MYDGF_KD_TMT6_s04.raw	Raw

Items per page:

1 - 5 of 73

Similar Datasets

Super-SILAC-based quantitative proteomic analysis of lung adenocarcinoma associated with stage and EGFR gene status

Project description:Lung adenocarcinoma (LUAD) is one of the most common causes of cancer death worldwide. Epidermal growth factor receptor (EGFR) mutations (MT) frequently target LUAD patients in Eastern Asia. EGFR tyrosine kinase inhibitors were developed to benefit LUAD patients harboring EGFR-activating MT. Unfortunately, biomarkers for early diagnosis and targeted therapy for patients with wild-type (WT) EGFR are currently lacking. Based on the super-SILAC, this study established a LUAD proteomics data set related to stage and EGFR status. Specifically, proteins obtained from three locally established LUAD cell lines were pooled with LUAD tissues from women, never smokers, different histological stages (early and late), and EGFR status (wild-type and mutant) to establish a quantitative proteome data set. We integrated genomic datasets and proteomic resources to select marker candidates for further characterization via immunohistochemistry and ELISA assays. The biological significance of marker candidates was examined using cell lines. This study provides new insights into the diagnosis and tumorigenesis of LUAD with EGFR-WT.

2025-06-05 | PXD046807 | Pride

RNAseq of combined LUAD and SCLC tumors to look at gene expression changes

Project description:For in-depth characterization of neuroendocrine transformation, we analyzed clinical specimens consisting of combined lung adenocarcinoma (LUAD)/small cell lung carcinoma (SCLC) histology exhibiting clear spatial separation. Microdissection was performed for RNA sequencing.

2021-06-03 | E-MTAB-10399 | biostudies-arrayexpress

Study the differential gene expression of different lung cancer EGFR mutants in NIH3T3 cells

Project description:Oncogenic mutations in the EGFR gene account for 15-20% of lung adenocarcinoma (LUAD) cases. However, the mechanism for EGFR driven tumor development and growth is not fully understood. Here, using a mRNA expression profiling-based approach we identified betacellulin (BTC) as one the gene upregulated by oncogenic EGFR in a MAP kinase-dependent manner. BTC protein expression was markedly increased in LUAD patient samples compared to normal lung tissue, with higher expression in EGFR-mutant LUAD. BTC was sufficient to transform immortalized mouse cells, initiate tumor development in mice, and promote the survival of immortalized human lung epithelial cells. Conversely, knockdown of BTC inhibited the growth of EGFR-mutant human LUAD cells in culture and their tumor-forming ability in mice. Mechanistically, BTC knockdown resulted in attenuated EGFR signaling and apoptosis induction. Collectively, these results demonstrate a key role of BTC in EGFR-mutant LUAD, with potential therapeutic implications in LUAD and other EGFR-mutant cancers.

2022-04-04 | GSE101399 | GEO

DNAJC5 facilitates the proliferation and migration of lung adenocarcinoma cells by augmenting EGFR trafficking

Project description:Lung adenocarcinoma (LUAD) is a highly prevalent and lethal malignant tumor, with the aberrantly activated EGFR signaling pathway playing a crucial role in its development. However, resistance to tyrosine-kinase inhibitors (TKIs) targeting EGFR significantly limits the efficacy of LUAD clinical therapy. Therefore, it is imperative to identify novel therapeutic targets and elucidate the regulatory mechanisms of EGFR for improving LUAD treatment outcomes. In this study, we discovered that DNAJC5 functions as an oncogene in LUAD. We observed elevated protein levels of DNAJC5 in tissues from LUAD patients, which were strongly associated with poor prognosis among these individuals. Furthermore, overexpression of DNAJC5 promoted proliferation and migration of LUAD cells both in vitro and in vivo. Mechanistic investigations revealed that DNAJC5 interacts with the intracellular domain of EGFR and enhances its endocytosis and recycle, thereby augmenting EGFR activity and downstream signaling pathways. Additionally, we found that DNAJC5 binds to AP2A1 protein—a key player in EGFR endocytosis—and strengthens its interaction with EGFR. Knockdown experiments targeting AP2A1 attenuated the ability of DNAJC5 to promote proliferation and migration of LUAD cells. Collectively, our findings unveil a functional role for DNAJC5 in regulating EGFR trafficking and driving LUAD progression.

2025-05-26 | PXD063682 | Pride

Detecting small cell transformation in patients with advanced EGFR mutant lung adenocarcinoma through epigenomic cfDNA profiling

Project description:Histologic transformation to small cell lung cancer (SCLC) is an increasingly common resistance mechanism to EGFR tyrosine kinase inhibitors in EGFR mutant lung adenocarcinoma (LUAD) that is underdiagnosed in clinical practice due to the requirement for tissue biopsy. Early and accurate detection of transformed (t)SCLC has important prognostic and therapeutic implications. To address this unmet need, we first comprehensively profiled the epigenomes of metastatic lung tumors finding widespread epigenomic reprogramming during histologic transformation from LUAD to SCLC. We then utilized a novel approach for epigenomic profiling of cell-free DNA, which discriminated patients with EGFR mutant tSCLC from patients with EGFR mutant LUAD with greater than 90% accuracy. This first demonstration of the ability to accurately, and non-invasively, detect small cell transformation in patients with EGFR mutant LUAD through epigenomic cfDNA profiling is a critical step towards a new paradigm of diagnostic and therapeutic precision for patients with advanced lung cancer.

2024-06-20 | GSE269746 | GEO

Gene expression profiling of FUT8 knockdown CL1-5 cells

Project description:Overexpression of fucosyltransferase 8 (FUT8) is found in many cancers including liver, ovarian, thyroid, colorectal and non-small cell lung cancers. Unlike other FUTs which are functionally redundant, FUT8 is the only enzyme responsible for the alpha1,6-linked fucosylation (core fucosylation) by adding fucose to the innermost GlcNAc residue of an N-linked glycan. A growing body of evidence indicates that core fucosylation is important for regulating protein functions, such as EGFR, TGF beta receptor and integrins. To understand the downstream molecular events in response to the global alteration of core fucosylation during cancer progression, microarray analysis was employed to profile the changes in gene expression following FUT8 silencing. The genes significantly (2-fold, P<0.01) changed in CL1-5/shFUT8 cells were selected for functional annotations using a Gene Ontology database. The result revealed that many genes involved in cell adhesion, motility, growth, angiogenesis, and inflammation were under the control of core fucosylation. In this experiment, the gene expression profile of two stable FUT8 knockdown clones of CL1-5 cells, CL1-5/shFUT8-1 and CL1-5/shFUT8-2, were compare with CL1-5/Control cells. A total of eight samples were analyzed, including four CL1-5/Control vs. CL1-5/shFUT8-1 and four CL1-5/Control vs. C1-5/shFUT8-2. The biological replicates for each cell lines were four.

2012-12-07 | E-GEOD-42405 | biostudies-arrayexpress

Integrative multi-omic analysis of the SWI/SNF complex defines a new clinical subgroup of lung adenocarcinoma patients

Project description:Mammalian SWI/SNF complexes are ATP-dependent chromatin remodelers composed of varying combinations of subunits that, together, fine-tune transcriptional regulation and genome integrity. SWI/SNF complex subunits have been identified as major targets of mutations in several tumor types suggesting a relevant role in tumorigenesis. However, there is a lack of comprehensive studies of the whole SWI/SNF complex in lung adenocarcinoma (LUAD). Here, we combined genomic, transcriptomic, and proteomic approaches to identify which SWI/SNF subunits are present in lung cells, as well as their mutational status, mRNA levels, and protein levels in LUAD. For these purposes, we combined data from LUAD primary tumors, normal lung and LUAD cell lines, and external LUAD data from The Cancer Genome Atlas. Importantly, we found that mutations in the SWI/SNF complex in LUAD not only present a high incidence but we also observed that only the mutational status of the SWI/SNF complex and not the mutations in any of the top ten LUAD driver genes is associated with poorer overall survival in LUAD patients. Furthermore, we showed that the expression of the SWI/SNF complex in LUAD suffers an overall repression that cannot be explained exclusively by genetic alterations. Based on our findings, we propose that SWI/SNF-mutant LUAD tumors should be considered as a distinct subgroup with practical applications in the prognosis and follow-up of LUAD patients.

2022-04-01 | PXD017397 | Pride

APOBEC mutagenesis and copy number alterations are drivers of proteogenomic tumor evolution and heterogeneity in metastatic thoracic tumors

Project description:Intratumor mutational heterogeneity has been documented in primary non-small cell lung cancer. Here, we elucidate mechanisms of tumor evolution and heterogeneity in metastatic thoracic tumors (lung adenocarcinoma and thymic carcinoma) using whole-exome and transcriptome sequencing, SNP array for copy number alterations (CNA) and mass spectrometry-based quantitative proteomics of metastases obtained by rapid autopsy. APOBEC-mutagenesis, promoted by increased expression of APOBEC3 region transcripts and associated with a high-risk germline APOBEC3 variant, strongly correlated with mutational tumor heterogeneity. TP53 mutation status was associated with APOBEC hypermutator status. Interferon pathways were enriched in tumors with high APOBEC mutagenesis and IFN- induced expression of APOBEC3B in lung adenocarcinoma cells in culture suggesting a role for the immune microenvironment in the generation of mutational heterogeneity. CNA occurring late in tumor evolution correlated with downstream transcriptomic and proteomic heterogeneity, although global proteomic heterogeneity was significantly greater than transcriptomic and CNA heterogeneity. These results illustrate key mechanisms underlying multi-dimensional heterogeneity in metastatic thoracic tumors.

2019-05-07 | PXD012845 | Pride

Glycoproteomics revealed novel N-glycosylation biomarkers for early diagnosis of lung adenocarcinoma cancers

Project description:Circulating biomarkers play important roles in diagnosis of malignant tumors. N-glycosylation is an important post-translation patter and obviously affect biological behaviors of malignant tumor cells. However, the role of N-glycosylation sites in early diagnosis of tumors still remains further investigation. In this study, plasma from 20 lung adenocarcinoma (LUAD), which were all classified as stage I, as well as 20 normal controls (NL) were labeled and screened by mass spectrometry (MS). Total 39 differential N-glycosylation sites were detected in LUAD, 17 were up-regulated and 22 were down-regulated. In all differential sites, ITGB3-680 showed highest potential in LUAD which showed 99.2% AUC, 95.0% SP and 95.0% SN. Besides, APOB-1523 (AUC: 89.0%, SP: 95.0%, SN: 70.0%), APOB-2982 (AUC: 86.8%, SP: 95.0%, SN: 45.0%) and LPAL2-101 (AUC: 81.1%, SP: 95.0%, SN: 47.4%) also acted as candidate biomarkers in LUAD. Combination analysis was then performed by random forest model, all samples were divided into training group (16 cases) and testing group (4 cases) and conducted by feature selection, machine learning, integrated model of classifier and model evaluation. And the results indicated that combination of differential sites could reach 100% AUC in both training and testing group. Taken together, our study revealed multiple N-glycosylation sites which could be applied as candidate biomarkers for early diagnosis diagnosis of LUAD.

2023-03-11 | PXD036198 | Pride

RBM10 Deficiency Promotes Brain Metastasis by Modulating Sphingolipid Metabolism in an Animal Model of EGFR Mutation Lung Adenocarcinoma

Project description:Brain metastasis significantly contributes to the failure of targeted therapy in patients with EGFR-mutated lung adenocarcinoma (LUAD). Reduced expression of RBM10 is associated with brain metastasis in these patients. However, the mechanism by which RBM10 affects brain metastasis in EGFR-mutated LUAD remains unclear. Previous studies reveal that RBM10 mutations lead to decreased expression and deregulated splicing at a subset of junctions, primarily through exon skipping.

2025-03-19 | GSE280915 | GEO

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