Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

EEF1D stabilized by SRSF9 promotes colorectal cancer via enhancing the proliferation and metastasis

ABSTRACT: Colorectal cancer is a common cancer and causes high mortality worldwide. It is urgent to explore its pathogenesis and seek effective therapeutic strategies. Here, the author showed that EEF1D expression in colorectal cancer cells is required to promote tumor growth and metastasis. Moreover, we further performed the proteomic analysis to gain a deeper mechanistic understanding of EEF1D in CRC. We found that EEF1D interacted with various cancer-related proteins. These interactions further support the importance of EEF1D in colorectal cancer.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Zhaopeng Yan

LAB HEAD: Zhaopeng Yan

PROVIDER: PXD047265 | Pride | 2024-05-02

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	HFX_LFQ_QWL022_EEF1D.raw	Raw
	HFX_LFQ_QWL022_EEF1D_PeptideGroups.xlsx	Xlsx
	HFX_LFQ_QWL022_IgG.raw	Raw
	HFX_LFQ_QWL022_IgG_PeptideGroups.xlsx	Xlsx

Items per page:

1 - 4 of 4

Similar Datasets

RNA-seq of human NSCL cell lines with induced fusion genes; ALK-EML4-V1, ALK-EML4-V3, ALK-TFG, ALK-KIF5B

Project description:To characterize the effects of common ALK fusion genes, we performed a comprehensive RNA-Seq analysis of NL20 cells induced with ALK-EML4-V1, ALK-EML4-V3, ALK-TFG, ALK-KIF5B, using Doxycycline

2022-12-18 | E-MTAB-11304 | biostudies-arrayexpress

Profiling of ADAM12S regulated proteins in H1688 cells

Project description:In this project, we used SILAC quantitative proteomics to identify proteins that are differentially regulated by the short secreted form of A Disintegrin And Metalloproteinase 12, ADAM12S, in a small cell lung cancer cell line H1688. The aim of this study is to discover the proteins that are responsible for the cell proliferation, migration, and invasion and then to elucidate the molecular mechanism by which ADAM12S promotes these processes in small cell lung cancer cells.

2021-02-15 | PXD013242 | Pride

SILAC quantification of proteins in the control and UFBP1-expressing MGC803 cells

Project description:In this project, we used SILAC quantitative proteomics to identify proteins that are differentially regulated by UFM1-binding and PCI domain-containing protein 1 (UFBP1, also called DDRGK domain-containing protein 1 or DDRGK1) in a gastric cancer cell line. The aim of this study is to discover the proteins that are responsible for the biological function of UFBP1.

2021-02-15 | PXD013590 | Pride

Methylation profiling by array shows that mIDH-associated DNA hypermethylation in acute myeloid leukemia reflects differentiation blockage rather than inhibition of TET-mediated demethylation

Project description:Isocitrate dehydrogenases 1 and 2 (IDH1/2) are recurrently mutated in acute myeloid leukemia (AML), but their mechanistic role in leukemogenesis is poorly understood. The inhibition of TET enzymes by D-2-hydroxyglutarate (D-2-HG), which is produced by mutant IDH1/2 (mIDH1/2), has been suggested to promote epigenetic deregulation during tumorigenesis. In addition, mIDH also induces a differentiation block in various cell culture and mouse models. Here we analyze the genomic methylation patterns of AML patients with mIDH using Infinium 450K data from a large AML cohort and found that mIDH is associated with pronounced DNA hypermethylation at tens of thousands of CpGs. Interestingly, however, myeloid leukemia cells overexpressing mIDH, cells that were cultured in the presence of D-2-HG or TET2 mutant AML patients did not show similar methylation changes. In further analyses, we also characterized the methylation landscapes of myeloid progenitor cells and analyzed their relationship to mIDH-associated hypermethylation. Our findings identify the differentiation state of myeloid cells, rather than inhibition of TET-mediated DNA demethylation, as a major factor of mIDH-associated hypermethylation in AML. Furthermore, our results are also important for understanding the mode of action of currently developed mIDH inhibitors.

2017-09-15 | E-MTAB-6059 | biostudies-arrayexpress

PDK1 Signaling Towards PLK1-Myc Activation Confers Oncogenic Transformation and Tumor Initiating Cell Activation and Resistance to mTOR-targeted Therapy.

Project description:Although 3-Phosphoinositide-dependent protein kinase-1 (PDK1) has been predominately linked to PI3K-AKT pathway, it may also evoke additional signaling outputs to promote tumorigenesis. Here we report that PDK1 directly induces phosphorylation of Polo-like kinase 1 (PLK1), which in turn induces Myc phosphorylation and protein accumulation. We show that PDK1-PLK1-Myc signaling is critical for cancer cell growth and survival and small molecule inhibition of PDK1/PLK1 provides an effective approach for therapeutic targeting Myc-dependency. Intriguingly, PDK1-PLK1-Myc signaling induces an embryonic stem cell-like gene signature associated with aggressive tumor behaviors and is a robust signaling axis driving cancer stem cell (CSC) self renewal. Finally, we show that PLK1 inhibitor synergizes with mTOR inhibitor to induce synergistic anti-tumor effect in colorectal cancer by antagonizing a compensatory Myc induction. These findings identify a novel pathway in human cancer and CSC activation and provide a therapeutic strategy for targeting Myc-associated tumorigenesis and therapeutic resistance. Gene expression profiling of Human Embryonic Kidney Cells (HEK-TERV) under different conditions: PMN, PDK1, MYC and E545K

2013-07-31 | E-GEOD-30669 | biostudies-arrayexpress

Overexpression of Mitochondrial Aconitase in HT29 Colon Cancer Cells Attenuates beta-Catenin Signaling Pathway via Metabolic Changes of NADPH and ROS

Project description:Our previous proteomics analysis suggested down-regulation of mitochondrial aconitase (ACO2) plays an important role in colorectal cancer. To evaluate the effect of mitochondrial aconitase overexpression on the metabolic and signaling pathway changes in colon cancer cell line HT29, we generated two ACO2 overexpressing cell lines #C and #UD and the mock-transfected vector control #VE. HT29 colon cancer cells overexpressing ACO2 exhibited lower rate of cell proliferation in vitro and reduced tumor growth potential in nude mice. In order to understand the signaling pathway changes, cDNA microarray analysis using GeneChips from Affymetrix were carried out.

2010-01-14 | E-MEXP-1996 | biostudies-arrayexpress

Genome-wide total RNA and MBD-sequencing in HCT116 and DKO cells as a global re-expression model [MBD-Seq]

Project description:Genome-wide view of the interplay between methylation and RNA expression in this colorectal cancer model was obtained. MBD-sequencing of 8 colorectal cancer cell lines.

2013-10-01 | E-GEOD-45333 | biostudies-arrayexpress

Expression data from colorectal cancer and liver metastasis

Project description:To identify the driver factors in liver metastasis of colorectal cancer, and seek for possible biomarkers, we applied array trascriptome detection using approaches tailored to FFPE derived RNA Integrated analysis identified metastasis related genes with potentially high clinical significance.

2016-12-02 | GSE72718 | GEO

mRNA-seq for HCT116 Parental and ARID1A knockdown cells, mRNA-seq for DLD1 Parental, ARID1A knockdown and ARID1A knockout cells, mRNA-seq for COLO320DM Parental and ARID1A knockdown and ARID1A knockout cells

Project description:The study identifies genes that are regulated by the loss of the chromatin remodeller subunit ARID1A in colorectal cancer cell lines. This gene is frequently mutated in colorectal cancer.

2019-06-11 | E-MTAB-7791 | biostudies-arrayexpress

HIGHLY EXPRESSED GENES IN RAPIDLY PROLIFERATING TUMOR CELLS AS NEW TARGETS FOR COLORECTAL CANCER TREATMENT

Project description:The clinical management of colorectal cancer patients has significantly improved due to the identification of new chemotherapeutic targets. Since rapid tumor proliferation is associated with poor patient prognosis, here we characterize the transcriptional signature of rapidly proliferating colorectal cancer cells in an attempt to identify novel candidate therapeutic targets. Therefore, the doubling time of 52 colorectal cancer cell lines was determined and genome-wide expression profiling of a subset of 31 of these cell lines was assessed by microarray analysis.

2015-05-13 | E-MTAB-2971 | biostudies-arrayexpress