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LKB1 regulates the transcriptome of immortalized endometrial cells

ABSTRACT: List of differentially-expressed transcripts following LKB1 knockdown with two non-overlapping shRNA constructs.

ORGANISM(S): Homo sapiens

PROVIDER: GSE67629 | GEO | 2015/04/08

SECONDARY ACCESSION(S): PRJNA280512

REPOSITORIES: GEO

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LKB1 regulates the transcriptome of immortalized endometrial cells

Project description:List of differentially-expressed transcripts following LKB1 knockdown with two non-overlapping shRNA constructs. Immortalized endometrial cells were stably transfected with two non-overlapping shRNA constructs (408-shRNA1, 409-shRNA2) and a non-target reference control (NT). RNA was harvested from dividing cells and loaded onto the Illumina HumanHT-12 v4 Expression BeadChip.

2015-04-08 | E-GEOD-67629 | biostudies-arrayexpress

SUMOylation regulates nucleo-cytoplasmic shuttling of LKB1 in liver cancer

Project description:Even though liver kinase B1 (LKB1) is commonly described as a tumor suppressor, we and others have shown that LKB1 is augmented in liver cancer. In agreement, LKB1 modulation in human hepatoma cells and mouse livers induces changes in cell proliferation and the appearance of liver neoplastic lesions in association with disruptions of energetic metabolism. After LKB1 overexpression, a surprising uncoupling between LKB1 and its downstream kinase AMP-activated protein kinase is observed as well as activation of the oncogenic Ras pathway, driven by the direct or indirect binding of LKB1 to the promoter region of the Ras activator, RASGRP3. Under these circumstances, LKB1 SUMOylation at Lys178 by SUMO-2, the main SUMO paralogue present in liver, promotes LKB1 nuclear localization, fueling hepatoma cell proliferation. Overall, SUMO-2 mediated modification of LKB1 at Lys178 is suggested as a bona fide oncogenic driver in liver cancer by regulating the nucleo-cytoplasmic shuttling of LKB1.

2018-09-11 | GSE99584 | GEO

Gene expression profiling associated with knockdown of LKB1 in human intrahepatic cholangiocarcinoma

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

Transcription profiling of Mus musculus gastric Lkb1 polyps vs unaffected gastric Lkb1 mucosa

Project description:Gene expression in wildtype mouse stomach wall (n=6), Lkb1+/- mouse stomach wall (n=6) and Lkb1+/- mouse gastric polyps

2010-10-06 | E-MEXP-2444 | biostudies-arrayexpress

Expression data for human acute myeloid leukemia KG1a cells and KG1a LKB1 gene knock down cells

Project description:To explore the function and signaling pathway of LKB1 gene in maintaining the characteristics of leukemic stem cells, we use shRNA to knock down(KD) the expression of LKB1 gene at the human acute myeloid leukemia KG1a cells which is CD34+CD38- and shows some of the characteristics of leukemic stem cells. Gene expression profile was used to analysis the difference gene expression in LKB1-KD KG1a cells and negative control (NC) KG1a cells.

2017-12-31 | GSE84904 | GEO

LKB1 modulates lung cancer differentiation and metastasis

Project description:Inherited mutation in LKB1 results in the Peutz-Jeghers syndrome (PJS), characterized by intestinal hamartomas and a modestly increased frequency of gastrointestinal and breast cancer1. Somatic inactivation of LKB1 occurs in human lung adenocarcinoma2-4, but its tumor suppressor role in this tissue is unknown. Here we show that somatic Lkb1 deficiency strongly cooperates with somatic K-rasG12D activating mutation to accelerate the development of mouse lung tumorigenesis. Lkb1 deficiency in the setting of K-rasG12D mutation (K-ras Lkb1L/L) was associated with decreased tumor latency and increased tumor aggressiveness including metastasis. Furthermore, tumors from K-ras Lkb1L/L mice demonstrated histologies--squamous, adenosquamous and large cell--not seen with K-rasG12D mutation, Ink4a/Arf inactivation, or p53 inactivation alone or in combination. Experiments in vitro suggest that LKB1 suppresses lung tumorigenesis and progression through both p16INK4a-ARF-p53 dependent and independent mechanisms. These data indicate that LKB1 regulates lung tumor progression and differentiation. Keywords: cancer research To analyze the role of LKB1 in lung cancer progression and differentiation, we have dissected the lung tumors from mice with/without lkb1 loss and performed the microarray analyses to compare their gene expression pattern. In addition, we have also performed microarray analysis in both A549 and H2126 cell lines after reconsistitution of either wt-lkb1 or the kinase dead form of lkb1 (lkb1-KD) to confirm what we observed from in vivo studies.

2007-08-28 | E-GEOD-6135 | biostudies-arrayexpress

LKB1 and Notch deletion in mouse liver

Project description:We characterize the phenotype of mice in which the deletion of Lkb1 has been targeted in the liver. Lack of Lkb1 in the liver results in bile duct paucity leading to cholestasis. This phenotype is similar to that obtained upon inactivation of Notch signaling in the liver. We test the hypothesis of a functional overlap between the Lkb1 and Notch pathways by gene expression profiling of livers deficent in Lkb1 or in the Notch mediator RbpJÎº. We used AlfpCre mice for liver-specific deletion of LKB1 that were crossed with a conditional knockout mouse model (LKB1 floxed mice). We used also AlfpCre mice for liver-specific inactivation of the Notch pathway. AlfpCre mice were crossed with the RbpJÎº floxed mice. RNA was extracted from the liver of LKB1 KO mice (Lkb1Floxed, AlfpCre positive mice) and their wild-type counterpart (Lkb1Floxed, AlfpCre negative mice). RNA was also extracted from liver of RbpJK KO mice (RbpJK floxed, AlfpCre positive) and their wild type mice (RbpJK floxed, AlfpCe negative). 6 samples for the liver-specific deletion of LKB1 corresponding to 3 KO LKB1 (Cre positive) and 3 normal liver (Cre negative). 6 samples for the liver-specific inactivation of the Notch pathway corresponding to 3 KO RbpJk (Cre positive) and 3 normal liver (Cre negative).

2015-12-08 | E-GEOD-75564 | biostudies-arrayexpress

LKB1-deficient and LKB1-reconstituted A549 NSCLC cells

Project description:LKB1-deficient and LKB1-reconstituted A549 NSCLC cells

| PRJNA529192 | ENA

RNA-seq profiling of WT, LKB1 KO, and LKB1/CRTC2 KO mouse embryonic fibroblasts

Project description:Investigating transcriptional profile of WT, LKB1 KO, and LKB1/CRTC2 KO mouse embryonic fibroblasts untreated or stimulated with IL-1β

2023-05-11 | GSE214823 | GEO

Examination of the role of peptidylarginine deiminase 2 (PAD2) in gene expression in MCF-7 breast cancer cells

Project description:To investigate the potential role of peptidylarginine deiminase 2 (PAD2) in gene expression, we created stable shRNA scrambled control and PAD2 knockdown MCF-7 breast cancer cell lines. After validating the specific knockdown of PAD2 at the mRNA and protein level, we utilized an Agilent microarray platform to compare the gene expression profile of the two cell lines to generate a candidate list of genes regulated by PAD2. Control and PAD2 knockdown cells were created by stably transfecting shRNA constructs into MCF-7 cells. Stable cells were selected using puromycin and knockdown validate at the mRNA and protein level. Microarray data represents 4 independent biological replicates contain control and PAD2 knockdown samples.

2012-04-06 | E-GEOD-37087 | biostudies-arrayexpress

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