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Gene expression changes induced by LKB1 expression in human lung adenocarcinoma cell lines

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Carbone David

PROVIDER: S-ECPF-GEOD-51266 | biostudies-other |

REPOSITORIES: biostudies-other

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Gene expression changes induced by LKB1 expression in human lung adenocarcinoma cell lines

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

Gene expression changes induced by LKB1 expression in human lung adenocarcinoma cell lines

2013-10-01 | E-GEOD-51266 | biostudies-arrayexpress

Changes in apoptotic gene expression induced by the DNA cross-linkers epichlorohydrin and diepoxybutane in human cell lines.

Project description:Real time quantitative reverse transcription PCR was used to monitor changes in apoptotic gene expression after treating cells with the DNA cross-linkers epichlorohydrin (ECH) and diepoxybutane (DEB). This article presents the data obtained from application of the comparative CT method to the amplification of twelve apoptotic genes in human MCF10-A cells and eight genes in HUVEC cells. Further insight regarding the significance of these data can be found in "Cross-linking by epichlorohydrin and diepoxybutane correlates with cytotoxicity and leads to apoptosis in human leukemia (HL-60) cells" (Le et al., 2018) [1].

| S-EPMC5998169 | biostudies-literature

Expression profiling of ubiquitin-related genes in LKB1 mutant lung adenocarcinoma.

Project description:Liver kinase B1 (LKB1) is a tumor suppressor, and there is a very high proportion of LKB1 mutation in lung adenocarcinoma. The function of LKB1 is closely related to that of ubiquitin related genes. Our objective is to analyze the changes in ubiquitin-related genes in LKB1 mutant lung adenocarcinoma. We searched The Cancer Genome Atlas (TCGA) and obtained gene expression profiles from 230 lung adenocarcinoma patients, which were then analyzed using R software. Kaplan-Meier curves and Cox proportional hazards regression were applied to estimate survival. Real-time reverse transcription PCR was used to verify gene expression. Gene function was explored by gene set enrichment analysis. There were significantly expressed differences in the ubiquitin-related gene SH3RF1 between the LKB1 mutant and wild-type lung adenocarcinoma patients (p?=?9.78013E-05). Patients with LKB1 mutation and high expression of SH3RF1 had a better prognosis than the low expression group (HR 0.356, 95% CI 0.136-0.929, p?=?0.035). SH3RF1 can influence cell cycle, apoptosis, DNA replication and the p53 signaling pathway. SH3RF1 might have great clinical value act as a diagnostic biomarker and indicator to evaluate the prognosis of LKB1 mutant lung adenocarcinoma patients. This gene also can become a new treatment target for LKB1 mutant lung adenocarcinoma patients.

| S-EPMC6125361 | biostudies-literature

LKB1/STK11 Expression in Lung Adenocarcinoma and Associations With Patterns of Recurrence.

Project description:BackgroundMutations in the serine/threonine kinase 11 (STK11)/liver kinase B1 (LKB1) have been implicated in mediating resistance to checkpoint blockade among patients with advanced lung adenocarcinoma. We sought to examine the associations between clinicopathologic characteristics, tumor LKB1 expression, features of the immune microenvironment, and postoperative prognosis among patients with early stage lung adenocarcinoma undergoing surgical therapy.MethodsFormalin-fixed, paraffin-embedded specimens of patients undergoing resection of stage I to III, chemotherapy-naïve adenocarcinomas (1997 to 2008) were analyzed using tissue microarray sectioning. Sublobar resections were excluded. Intratumoral LKB1/STK11 expression was quantified as H-score. In a subset, tumor-associated immune cell populations were quantified using whole tumor sections in peritumoral and intratumoral compartments.ResultsIn all, 104 patients met inclusion criteria. Expression of LKB1/STK11 (median H-score 102.9) was higher in women (median 123.3) than in men (100, P = .004) and in never-smokers (median 145) than in former/current smokers (100, P = .002). Expression of LKB1/STK11 was positively correlated with intratumoral infiltration of cluster of differentiation (CD) 3+ (r = 0.351, P = .005), CD4+ (r = 0.436, P < .001), and CD8+ (r = 0.263, P = .049) cells. Patients with extrathoracic recurrence had lower tumor expression of LKB1/STK11 than did other patients with recurrent disease. On multivariate analysis, low LKB1/STK11 expression remained independently associated with poor disease-free survival and distant disease-free survival.ConclusionsLow LKB1/STK11 expression is associated with specific patient characteristics and poor postoperative prognosis in chemotherapy-naïve lung adenocarcinoma. Further investigation is warranted to delineate its clinical significance in the context of evaluating novel therapeutic agents in patients with resectable disease.

| S-EPMC8215648 | biostudies-literature

Gene expression profiling of cancer stem cell in human lung adenocarcinoma A549 cells.

Project description:BackgroundThe studies on cancer-stem-cells (CSCs) have attracted so much attention in recent years as possible therapeutic implications. This study was carried out to investigate the gene expression profile of CSCs in human lung adenocarcinoma A549 cells.ResultsWe isolated CSCs from A549 cell line of which side population (SP) phenotype revealed several stem cell properties. After staining the cell line with Hoechst 33342 dye, the SP and non-side population (non-SP) cells were sorted using flow cytometric analysis. The mRNA expression profiles were measured using an Affymetrix GeneChip(R) oligonucleotide array. Among the sixty one differentially expressed genes, the twelve genes inclusive three poor prognostic genes; Aldo-keto reductase family 1, member C1/C2 (AKR1C1/C2), Transmembrane 4 L six family member 1 nuclear receptor (TM4SF1), and Nuclear receptor subfamily 0, group B, member 1 (NR0B1) were significantly up-regulated in SP compared to non-SP cells.ConclusionThis is the first report indicating the differences of gene expression pattern between SP and non-SP cells in A549 cells. We suggest that the up-regulations of the genes AKR1C1/C2, TM4SF1 and NR0B1 in SP of human adenocarcinoma A549 cells could be a target of poor prognosis in anti-cancer therapy.

| S-EPMC2234429 | biostudies-literature

Gene expression changes associated with Barrett's esophagus and Barrett's-associated adenocarcinoma cell lines after acid or bile salt exposure.

Project description:Esophageal reflux and Barrett's esophagus represent two major risk factors for the development of esophageal adenocarcinoma. Previous studies have shown that brief exposure of the Barrett's-associated adenocarcinoma cell line, SEG-1, or primary cultures of Barrett's esophageal tissues to acid or bile results in changes consistent with cell proliferation. In this study, we determined whether similar exposure to acid or bile salts results in gene expression changes that provide insights into malignant transformation.Using previously published methods, Barrett's-associated esophageal adenocarcinoma cell lines and primary cultures of Barrett's esophageal tissue were exposed to short pulses of acid or bile salts followed by incubation in culture media at pH 7.4. A genome-wide assessment of gene expression was then determined for the samples using cDNA microarrays. Subsequent analysis evaluated for statistical differences in gene expression with and without treatment.The SEG-1 cell line showed changes in gene expression that was dependent on the length of exposure to pH 3.5. Further analysis using the Gene Ontology, however, showed that representation by genes associated with cell proliferation is not enhanced by acid exposure. The changes in gene expression also did not involve genes known to be differentially expressed in esophageal adenocarcinoma. Similar experiments using short-term primary cultures of Barrett's esophagus also did not result in detectable changes in gene expression with either acid or bile salt exposure.Short-term exposure of esophageal adenocarcinoma SEG-1 cells or primary cultures of Barrett's esophagus does not result in gene expression changes that are consistent with enhanced cell proliferation. Thus other model systems are needed that may reflect the impact of acid and bile salt exposure on the esophagus in vivo.

| S-EPMC1925102 | biostudies-literature

Effects of PD-0332991 on gene expression of human pancreatic ductal adenocarcinoma (PDAC) cell lines

Project description:PD-0332991 is a small molecule inhibitor for Cdk4 and Cdk6. It exerted growth inhibitory effects on PDAC cell lines (AsPC-1 and COLO-357). Microarray analysis was used to characterize the changes in gene expression profiles of AsPC-1 and COLO-357 upon PD-0332991 incubation AsPC-1 and COLO-357 cells were treated in the absence or presence of 5 µM PD-0332991 for 24 h and 72 h. Each expreimental condition had biological triplicates. Twenty-four samples were analyzed in total.

| S-ECPF-GEOD-39646 | biostudies-other

human lung adenocarcinoma cell lines TMT based proteomics

Project description:In our study, we found that profilin 1 (PFN1) promoted non-small cell lung cancer (NSCLC) metastasis.For further investigate the mechanisms of PFN1's roles in NSCLC metastasis, we constructed PFN1 overxpression H1299 cell lines(H1299 PFN1 OE cells). And we sent samples of H1299 PFN1 OE cells and EV cells for TMT based quantative proteome profiling.

2022-04-14 | PXD033148 | Pride

Transdifferentiation of lung adenocarcinoma in mice with Lkb1 deficiency to squamous cell carcinoma.

Project description:Lineage transition in adenocarcinoma (ADC) and squamous cell carcinoma (SCC) of non-small cell lung cancer, as implicated by clinical observation of mixed ADC and SCC pathologies in adenosquamous cell carcinoma, remains a fundamental yet unsolved question. Here we provide in vivo evidence showing the transdifferentiation of lung cancer from ADC to SCC in mice: Lkb1-deficient lung ADC progressively transdifferentiates into SCC, via a pathologically mixed mAd-SCC intermediate. We find that reduction of lysyl oxidase (Lox) in Lkb1-deficient lung ADC decreases collagen disposition and triggers extracellular matrix remodelling and upregulates p63 expression, a SCC lineage survival oncogene. Pharmacological Lox inhibition promotes the transdifferentiation, whereas ectopic Lox expression significantly inhibits this process. Notably, ADC and SCC show differential responses to Lox inhibition. Collectively, our findings demonstrate the de novo transdifferentiation of lung ADC to SCC in mice and provide mechanistic insight that may have important implications for lung cancer treatment.

| S-EPMC3929783 | biostudies-literature

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