Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA356645 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The experiment was designed to display differential gene expression profiling changes in two human glioblastoma cells upon knockdow of LKB1 tumor suppressor, by using RNAseq technology.
2016-12-08 | GSE91016 | GEO
Project description:Global transcriptional changes in U87MG glioblastoma cells upon shRNA-mediated TRIM52 knockdown
| PRJNA421947 | ENA
Project description:The experiment was designed to display differential gene expression profiling in three human intrahepatic cholangiocarcinoma (ICC) cells upon knockdow of LKB1 tumor suppressor, by using RNAseq technology. LKB1 was first attenuated in three ICC cells: HuH-28, RBE, and SSP-25 by siRNA-mediated knockdown. Total RNA was extracted from duplicated cancers cells transfected with control siRNA and LKB1 specific siRNA at 48h posttransfection for RNAseq analysis. Differentially expressed genes in LKB1-attenuated ICC cells were identified in comparison to that in ICC cells transfected with control siRNA.
2014-07-29 | E-GEOD-59855 | biostudies-arrayexpress
Project description:Global transcriptional profiling changes upon knockdown of G9a in human non-small cell lung cancer cells
| PRJNA451303 | ENA
Project description:NEDD9 is important for lung cancer metastasis. However, the detailed mechanism remains elusive. Using the microarray data generated with human lung cancer cell lines with either NEDD9 overexpression or NEDD9 knockdown, we plan to idnetify important signal pathways regulated by NEDD9. This may explain how NEDD9 excutes its function in lung cancer. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process. Human lung cancer cell line A549, which has LKB1 loss-of-function mutation and increased expression of NEDD9, was used for two individual NEDD9 knockdown. Human lung cancer cell line CRL-5907, which has wild-type LKB1 and low NEDD9 expression level, was used for NEDD9 overexpression. The microarray was done in A549 cells, A549 cells with two different NEDD9 knockdown; CRL-5907 cells and CRL-5907 cells with NEDD9 overexpression.
2013-02-21 | E-GEOD-26846 | biostudies-arrayexpress
Project description:LKB1 is a tumor suppressor lost in approximately 30% of lung adenocarcinomas. It is a serine-threonine kinase involved in regulating metabolism, proliferation, and cell polarity. We have characterized its association with mRNA expression profiles in resected tumors and in cell lines, but little is known about the direct effects of LKB1 on the regulation of these genes. This study investigates the effects of LKB1 activity on mRNA expression in two LKB1-mutant lung adenocarcinoma cell lines, H2122 and A549. Wild-type LKB1 has been stably expressed in these cell lines using a pBABE retrovirus as well as an empty pBABE control and a kinase-dead mutant of LKB1 (K78I) control (Addgene). Samples submitted are two cell lines, three experimental conditions, and three replicates, for a total of 17 samples (one sample was excluded for poor RNA quality). Gene expression of these samples are analyzed to determine transcriptional regulatory effects of LKB1 expression. Results of this analysis are compared to our analysis of resected human tumors to determine gene patterns that are differentially expressed between LKB1-deficient and LKB1-wild-type tumors whose expression is also affected by restoration of LKB1 in vitro. RMA gene expression was taken from two cell lines stably expressing LKB1 or controls of K78I mutant LKB1 or empty pBABE vector. Log2 average expression differences are calculated and compared to results from analysis of gene expression associated with LKB1 loss in resected human tumors.
2013-10-01 | E-GEOD-51266 | biostudies-arrayexpress
Project description:This experiment analyzes the global proteome and phosphoproteome in YAP amplified cell lines upon YAP knockdown and/or MEK inhibition.
2020-03-17 | MSV000085111 | MassIVE
Project description:The experiment was designed to display differential gene expression profiling in three human intrahepatic cholangiocarcinoma (ICC) cells upon knockdow of LKB1 tumor suppressor, by using RNAseq technology.
2014-07-29 | GSE59855 | GEO
Project description:LKB1 is a tumor suppressor lost in approximately 30% of lung adenocarcinomas. It is a serine-threonine kinase involved in regulating metabolism, proliferation, and cell polarity. We have characterized its association with mRNA expression profiles in resected tumors and in cell lines, but little is known about the direct effects of LKB1 on the regulation of these genes. This study investigates the effects of LKB1 activity on mRNA expression in two LKB1-mutant lung adenocarcinoma cell lines, H2122 and A549. Wild-type LKB1 has been stably expressed in these cell lines using a pBABE retrovirus as well as an empty pBABE control and a kinase-dead mutant of LKB1 (K78I) control (Addgene). Samples submitted are two cell lines, three experimental conditions, and three replicates, for a total of 17 samples (one sample was excluded for poor RNA quality). Gene expression of these samples are analyzed to determine transcriptional regulatory effects of LKB1 expression. Results of this analysis are compared to our analysis of resected human tumors to determine gene patterns that are differentially expressed between LKB1-deficient and LKB1-wild-type tumors whose expression is also affected by restoration of LKB1 in vitro.
2013-10-01 | GSE51266 | GEO
Project description:The serine/threonine kinase LKB1 is a tumor suppressor gene which also plays key roles in metabolic function in peripheral tissues through its direct phosphorylation and activation of the AMP-activated protein kinase (AMPK). The LKB1/AMPK pathway plays key roles in the liver in suppressing transcriptional programs of gluconeogenesis and lipogenesis, and hepatic LKB1 is required for the ability of the type 2 diabetes agent metformin to lower blood glucose levels in mice. To more broadly define how the LKB1/AMPK pathway controls hepatic metabolism, transcriptional profiling was employed using mice with an inducible liver-specific deletion of Lkb1. Unexpectedly, LKB1/AMPK signaling broadly controls the expression of many phase I xenobiotic metabolism genes, including several members of the cytochrome P450 family. In particular, expression of CYP2E1, an important mediator of drug detoxification, was markedly reduced upon LKB1 loss. LKB1 liver-specific knockout mice exposed to hepatocarcinogens, exhibited marked resistance to carcinogen-induced hepatocyte apoptosis, proliferation, senescence, and liver fibrosis and tumorigenesis.
2019-05-01 | GSE21984 | GEO