Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MCT4 knockdown in pancreatic cancer cells

ABSTRACT: Gene expression levels were determined with control or MCT4 knockdown pancreatic cancer cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE63231 | GEO | 2014/12/17

SECONDARY ACCESSION(S): PRJNA267026

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

MCT4 knockdown in pancreatic cancer cells

Project description:Gene expression levels were determined with control or MCT4 knockdown pancreatic cancer cells. MiaPaca2, Capan-2, and PL45 cells were transfected with non-specific or MCT4-specific RNAi. RNA was harvested at 72 hours post transfection and analyzed on Illumina microarrays.

2014-12-17 | E-GEOD-63231 | biostudies-arrayexpress

DIA proteomics analysis of RNF223 knockdown and control pancreatic cancer cell lines

Project description:The proteome profiles of RNF223 knockdown and control pancreatic cancer cell lines were compared employing data independent acquisition(DIA) technology

2021-09-10 | PXD028446 |

Homo sapiens

Project description:MCT4 knockdown in pancreatic cancer cells

| PRJNA267026 | ENA

Next generation sequencing analysis of knockdown-Control and LINC00842-knockdown pancreatic cancer cell lines transcriptomes

Project description:Gene expression profiling of pancreatic cancer cell PANC-1 and SW1990 when LINC00842 knockdown by CRISPR/Cas9 system. We identified LINC00842 is a novel prognosis related lincRNA in pancreatic cancer and its regulation networks is poorly understood. We used the total RNA from knockdown control and LINC00842-knockdown PANC-1 and SW1990 cells to analyze the differentially expressed genes which were regulated by LINC00842, and further explored the biological processes that LINC00842 may involved.

2021-04-21 | GSE150216 | GEO

CD73 knockdown effect in pancreatic cancer cell lines

Project description:CD73 knockdown effect in pancreatic cancer cell lines

| PRJNA480855 | ENA

Next generation sequencing analysis of knockdown-Control and LINC00842-knockdown pancreatic cancer cell lines transcriptomes

Project description:Next generation sequencing analysis of knockdown-Control and LINC00842-knockdown pancreatic cancer cell lines transcriptomes

| PRJNA631529 | ENA

Pancreatic Cancer HPAF/CD18 cells: Ecd knockdown vs Scrambled

Project description:Purpose: To study the expression and function of a novel cell cycle regulatory protein, human ecdysoneless (Ecd), during pancreatic cancer (PC) pathogenesis. Experimental Design: Immunohistochemical expression profiling of Ecd was done in non-neoplastic normal pancreatic tissues and pancreatic ductal adenocarcinoma lesions (from tissue microarray and Rapid Autopsy program) as well as precancerous PanIN lesions and metastatic organs. To analyze the biological significance of Ecd in PC progression, Ecd was stably knocked down in PC cell line followed by in vitro and in vivo functional assays. Results: Normal pancreatic ducts show very weak to no Ecd expression compared to significant positive expression in PC tissues (mean±SE composite score: 0.3±0.2 and 3.8±0.2 respectively, p<0.0001) as well as in PanIN precursor lesions with a progressive increase in Ecd expression with increasing dysplasia (PanIN-1 to PanIN-3). Analysis of matched primary tumors and metastases from PC patients revealed that Ecd is highly expressed in both primary pancreatic tumor and in distant metastatic sites. Further, knockdown of Ecd suppressed cell proliferation in vitro and tumorigenicity of PC cells in mice orthotopic tumors. Microarray study revealed that Ecd regulates expression of glucose transporter GLUT4 in PC cells and was subsequently shown to modulate glucose uptake, lactate production and ATP generation by PC cells. Finally, knockdown of Ecd also reduced level of pAkt, key signaling molecule known to regulate aerobic glycolysis in cancer cells. Conclusion: Ecd is a novel tumor promoting factor that is differentially expressed in pancreatic cancer and potentially regulates glucose metabolism within cancer cells. Two-condition experiment, Ecd knockdown vs Scrambled cells. Biological replicates: 3 Ecd knockdownl, 3 Scrambled, independently grown and harvested. One replicate per array

2012-08-09 | E-GEOD-39988 | biostudies-arrayexpress

Induction of oxidative- and endoplasmic-reticulum-stress dependent apoptosis in pancreatic cancer cell lines by DDOST knockdown

Project description:The dolichyl-diphosphooligosaccharide-protein glycosyltransferase non-catalytic subunit (DDOST) is a key component of the oligosaccharyltransferase complex catalyzing N-linked glycosylation in the endoplasmic reticulum lumen. DDOST is associated with several cancers and congenital disorders of glycosylation. However, its role in pancreatic cancer remains elusive, despite its enriched pancreatic expression. Using quantitative mass spectrometry, we identify 30 differentially expressed proteins and phosphopeptides (DEPs) after DDOST knockdown in the pancreatic ductal adenocarcinoma (PDAC) cell line PA-TU-8988T. We evaluated DDOST / DEP protein-protein interaction networks using STRING database, correlation of mRNA levels in pancreatic cancer TCGA data, and biological processes annotated to DEPs in Gene Ontology database. The inferred DDOST regulated phenotypes were experimentally verified in two PDAC cell lines, PA-TU-8988T and BXPC-3. We found decreased proliferation and cell viability after DDOST knockdown, whereas ER-stress, ROS-formation and apoptosis were increased. In conclusion, our results support an oncogenic role of DDOST in PDAC by intercepting cell stress events and thereby reducing apoptosis. As such, DDOST might be a potential biomarker and therapeutic target for PDAC.

2024-09-03 | PXD047441 | Pride

TCF7L1 knockdown in pancreatic cancer

Project description:RNAi mediated depletion of TCF7L1 increases activity of a Wnt-based reporter and imparts more aggressive tumor phenotypes in vitro in pancreatic cancer cell lines that express TCF7L1. We sought to determine what changes in transcription ocurred after RNAi mediated knockdown of TCF7L1 in these cells by RNA-sequencing

2017-06-20 | GSE90926 | GEO

pancreatic cancer

Project description:pancreatic cancer

| PRJEB40742 | ENA