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Expression data from H358

ABSTRACT: Tumors that show evidence of epithelial to mesenchymal transition (EMT) have been associated with metastasis, drug resistance, and poor prognosis. EMT may alter the molecular requirements for growth and survival in different contexts, but the underlying mechanisms remain incomplete. Given the heterogeneity along the EMT spectrum between and within tumors it is important to define the requirements for growth and survival in cells with an epithelial or mesenchymal phenotype to maximize therapeutic efficacy. We have established an inducible cell line model in which a tamoxifen regulatable Twist-ER fusion protein is stably expressed in the H358 non-small cell lung cancer cell line. Upon tamoxifen addition, cells undergo EMT and provide a system in which we can compare the growth and survival requirements directly related to EMT, removing confounding factors present when comparing different cell lines.

ORGANISM(S): Homo sapiens

PROVIDER: GSE52308 | GEO | 2014/01/01

SECONDARY ACCESSION(S): PRJNA227364

REPOSITORIES: GEO

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Expression data from H358

Project description:Tumors that show evidence of epithelial to mesenchymal transition (EMT) have been associated with metastasis, drug resistance, and poor prognosis. EMT may alter the molecular requirements for growth and survival in different contexts, but the underlying mechanisms remain incomplete. Given the heterogeneity along the EMT spectrum between and within tumors it is important to define the requirements for growth and survival in cells with an epithelial or mesenchymal phenotype to maximize therapeutic efficacy. We have established an inducible cell line model in which a tamoxifen regulatable Twist-ER fusion protein is stably expressed in the H358 non-small cell lung cancer cell line. Upon tamoxifen addition, cells undergo EMT and provide a system in which we can compare the growth and survival requirements directly related to EMT, removing confounding factors present when comparing different cell lines. H358 cells stably expressing either GFP or TwistER were treated for 12 days in culture with 100nM 4-hydroxytamoxifen followed by RNA isolation. Three biological replicates of each condition were collected.

2014-01-01 | E-GEOD-52308 | biostudies-arrayexpress

Time course of TGFbeta induced epithelial mesenchymal transition (EMT) in H358 NSCLC cells.

Project description:Time course of TGFbeta induced epithelial mesenchymal transition (EMT) in H358 NSCLC cells.

| PRJNA515921 | ENA

Systems level analysis of epithelial to mesenchymal transition reveals more alteration in phosphoproteome than proteome and identifies DNAJB4 and CD81 as EMT regulators

Project description:We quantified protein expression changes between epithelial and mesechymal stages in immortalized human mammary epithelial cells (HMLE). Epithelial–mesenchymal transition is induced by expressing an EMT-TF, Twist.

2019-06-24 | PXD012001 | Pride

Epithelial-to-mesenchymal transition defines feedback activation of receptor tyrosine kinase signaling induced by MEK inhibition in KRAS mutant lung cancer

Project description:To determine the difference of gene expression profile in epithelial and mesenchymal KRAS mutant lung cancers, epithelial NCI-H358 cells were treated with TGFβ1 (4 ng/mL) or PBS for 14 days in order to induce epithelial to mesenchymal transition (EMT). Gene expression was determined in NCI-H358 cells before and after EMT induction. In addition, in order to investigate the effect of a MEK inhibitor trametinib on gene expression, mesenchymal NCI-H1792 cells were treated with 50 nM trametinib for 48 hours. Gene expression of H1792 cells for pre- and post-trametinib treatement was determined.

2017-03-15 | GSE79235 | GEO

An EMT-driven alternative splicing program occurs in human breast cancer and modulates cellular phenotype.

Project description:Regulation of cell-cell junction formation and regulation of cell migration were enriched among EMT (Epithelial-Mesenchymal Transition)-associated alternatively splicing events. Our analysis suggested that most EMT-associated alternative splicing events are regulated by one or more members of the RBFOX, MBNL, CELF, hnRNP or ESRP classes of splicing factors. The EMT alternative splicing signature was confirmed in human breast cancer cell lines, which could be classified into basal and luminal subtypes based exclusively on their EMTassociated splicing pattern. Expression of EMT-associated alternative mRNA transcripts was also observed in primary breast cancer samples, indicating that EMT-dependent splicing changes occur commonly in human tumors. The functional significance of EMT-associated alternative splicing was tested by expression of the epithelial-specific splicing factor ESRP1 or depletion of RBFOX2 in mesenchymal cells, both of which elicited significant changes in cell morphology and motility towards an epithelial phenotype, suggesting that splicing regulation alone can drive critical aspects of EMT-associated phenotypic changes. The molecular description obtained here may aid in the development of new diagnostic and prognostic markers for analysis of breast cancer progression. Examination of transcriptomes of HMLE/Twist-ER before and after induction of EMT by tamoxifen

2011-07-15 | E-GEOD-30290 | biostudies-arrayexpress

Gene expression profiling of NSCLC cell lines upon TGFb-induced epithelial-mesenchymal transition (EMT)

Project description:Epithelial-mesenchymal transition has been implicated in tumor metastasis, cancer drug resistance and cancer stem cell features. In this study, we examined gene expression profiles of three non-small cell lung cancer cell lines, before and after experimentally induced EMT. We modeled epitheial-mesenchyml transition by culturing A549, HCC827 and NCI-H358 cells in the presence of TGFb for three weeks, and compared gene expression profiles of the paretnal cells and cells after EMT.

2014-11-19 | E-GEOD-49644 | biostudies-arrayexpress

microRNA profiling of H358 non-small cell lung cancer cells selected for resistance against erlotinib or wild-type

Project description:Erlotinib is a tyrosine kinase inhibitor (TKI) that is approved as a second-line monotherapy in patients with advanced non-small cell lung cancer (NSCLC). In these patients, erlotinib prolongs survival but its benefit remains modest since overtime, many tumors develop resistance. To analyse the changes in the gene expression profile, that accompany resistance development, we treated the erlotinib sensitive non-small cell lung cancer cell line H358 with increasing concentrations of erlotinib (1-5µM) for several weeks (H358res). In parallel, we kept H358 with the same concentrations of the vehicle DMSO (H358co). After ten weeks of treatment, when the H358res stably grew under 5µM erlotinib, total RNA including microRNA of both cell lines was harvested and analyzed.

2015-09-15 | E-MTAB-3391 | biostudies-arrayexpress

Twist expression in HMLE and breast cancer T47D cells

Project description:Twist is a key EMT inducer, expression of Twist will induce EMT in HMLE and breast tumor T47D cells By expressing Twist in HMLE and T47D cells, which lack the expression of Twist, will identify the genes regulated by Twist

2013-12-12 | GSE53222 | GEO

Gene expression analysis of H358 non-small cell lung cancer cells selected for resistance against erlotinib or wild-type

2015-09-15 | E-MTAB-3387 | biostudies-arrayexpress

Regan2022 - Mechanosensitive EMT model with autocrine TGFbeta signaling

Project description:This model is an expansion of the Regan2022 - Mechanosensitive EMT model (MODEL2208050001); it includes a TGFβ signaling module and autocrine signaling in mesenchymal cells. The expanded 150-node (630 link) modular model undergoes EMT triggered by biomechanical and growth signaling crosstalk, or by TGFβ. As its predecessor, this model also reproduces the ability of the core EMT transcriptional network to maintain distinct epithelial, hybrid E/M and mesenchymal states, as well as EMT driven by mitogens such as EGF on stiff ECM. We also reproduce the observed lack of stepwise MET, in that our model's dynamics does not pass through the hybrid E/M state during MET. We show that in the absence of strong autocrine signals such as TGFβ (not included in this version), cells cannot maintain their mesenchymal state in the absence of mitogens, on softer matrices, or at high cell density. In contrast, potent autocrine signaling can stabilize the mesenchymal state in all but very dense monolayers on soft ECM. This expanded model also reproduces the inhibitory effects of TGFβ on proliferation and anoikis resistance in mesenchymal cells, as well as its ability to trigger apoptosis on soft ECM vs. EMT on stiff matrices. The model offers several experimentally testable predictions related to the effect of neighbors on partial vs. full EMT, the tug of war between mitosis and the maintenance of migratory hybrid E/M states, as well as cell cycle defects in dynamic, heterogeneous populations of epithelial, hybrid E/M and mesenchymal cells.

2023-12-13 | MODEL2208050002 | BioModels

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