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Transcriptomic analysis of APS organoids with and without EGF

ABSTRACT: EGF is the main mitogen promoting the growth of Kras WT colon cancer organoids. Here we aim to elucidate changes in expression profile of organoids in a suboptimal niche, mimicking the slow proliferation conditions that a tumor senses in vivo

ORGANISM(S): Mus musculus

PROVIDER: GSE187512 | GEO | 2022/05/12

REPOSITORIES: GEO

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Transcriptomic analysis of APS organoids with and without EGF

Project description:Transcriptomic analysis of APS organoids with and without EGF

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BRB-seq data of murine intestinal organoids treated with 100ng/ml of Egf, Ereg or Nrg1 ligand for 24 h

Project description:Regeneration of the intestinal epithelium is a dynamic process requiring a transient Yap-dependent reprogramming of the epithelium into a fetal-like state. Adjacent stroma, including subepithelial fibroblasts, are believed to coordinate the process, but mechanisms are not well understood. Here, we identify Neuregulin 1 (NRG1) and Epiregulin (EREG) as fibroblast-derived EGF ligands in colon and intestine which are induced during regeneration and capable of supporting the growth of the intestinal epithelium. While EREG stimulated intestinal organoid growth similarly to EGF, NRG1 increased de novo crypt formation. The goal of this experiment was to observe the differences in gene expression profile of stromal-derived EGF ligands EREG and NRG1 on intestinal organoids compared to traditional used EGF. Organoids were derived from intestinal crypts of a WT mice C57BL/6J. To exclude the size differences observed in long term cultures of EREG and NRG1, we first cultured the organoids for three days in normal ENR media, removed exogenous EGF for 24h and added EGF, EREG or NRG1 to the culture medium for 24 hours prior to the RNA isolation. NRG1 treated organoids acquired a fetal/regenerative transcriptome including activation of the Yap pathway and induction of epithelial EGF ligand Ereg and Amphiregulin (Areg) expression, highlighting the dynamic orchestration of the EGF signaling during regeneration.

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Genome-wide maps of H3K27ac ocupancy on chromatin in murine acinar cell line upon EGF treatment and Arid1a silencing

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EGF Induces Migration Independent of EMT or Invasion in A549 Lung Adenocarcinoma Cells

Project description:Tumors and tumor surrounding tissues produce multiple growth factors that influence tumor cell behavior via different signal transduction pathways. Growth factors like transforming growth factor beta (TGFβ) and epidermal growth factor (EGF) were shown to induce proliferation, migration and invasion in different cell models. Both factors are frequently overexpressed in cancer and will often act in combination. Although both factors are being used as rational targets in clinical oncology, similarities and differences of their contributions to cancer cell migration and invasion are not fully understood. Here we compared the impact of TGFβ, EGF and the combination of both factors on A549 cells. Both factors stimulated A549 migration to a similar extent but with a different kinetic and the combination had an additive effect. While EGF-induced migration depended on activation of the mitogen-activated protein kinase (MAPK) pathway, this pathway was dispensable for TGFβ-induced migration despite a strong activation by TGFβ. Proteome analysis revealed an overlap in expression patterns of migration-related proteins and associated gene ontology (GO) terms by TGFβ and EGF but only TGFβ induced the expression of epithelial to mesenchymal transition (EMT)-related proteins like matrix metalloproteinase 2 (MMP2). EGF in contrast, made no major contribution to EMT marker expression on either the protein or the transcript level. In line with these expression patterns, EGF was unable to increase invasion of A549 cells on its own and failed to enhance TGFβ-induced invasion. Overall, these data suggest that TGFβ and EGF may partly compensate each other for stimulation of cell migration but abrogation of TGFβ signaling may be more suitable for antagonizing invasion.

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SILAC identifies LAD1 as an oncogenic filamin binder regulating actin dynamics in response to EGF and marking aggressive breast tumors

Project description:Mutations mimicking growth factor-induced proliferation and motility characterize some aggressive subtypes of mammary tumors. To unravel novel players, we applied phosphoproteomics on untransformed mammary cells, which were pre-stimulated with the epidermal growth factor (EGF). This analysis identified ladinin-1 (LAD1), a hitherto poorly characterized protein, as a phosphor-effector of the EGF-to-ERK pathway. We report that LAD1 is essential for mammary cell proliferation and migration. LAD1 is transcriptionally induced, undergoes phosphorylation by EGF and co-localizes with actin stress fibers. Yeast 2-hybrids and co-immunoprecipitation screens revealed that LAD1 binds with filamins, actin cross-linking proteins. Co-sedimentation analyses attribute to LAD1 a role in actin treadmilling, probably in conjuction with SFN/14-3-3sigma. Depletion of LAD1 led to a decrease in viability related transcripts, and inhibited growth of mammary xenografts in an animal model. Furthermore, LAD1 is highly expressed in two aggressive subtypes of breast cancer, as well as predicts poor patient prognosis. These studies identify a new cytoskeletal component essential for signal transduction and for the acquisition of oncogenic attributes by human mammary tumors.

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HaCaT cells treated with bleogen pB1 or eGF

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EGF-induced Transcriptome Changes in GBM stem-like cells

Project description:GBM neurosphere line GBM1B were depleted of growth factors for 16 hours followed by EGF stimulation for 4 and 24 hours. RNA-seq was used to identify differentially-expressed (DE) genes after EGF treatment.

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Producing enteroendocrine cells from Lgr5+ intestinal stem cells by manipulating quiescence

Project description:Lgr5+ adult intestinal stem cells are highly proliferative throughout life. Single Lgr5+ stem cells can be cultured into 3D epithelial organoids containing all cell types at nearnormal ratios. Culture conditions to generate the main cell types have been established previously, but signals inducing the various types of enteroendocrine cells (EECs) have remained elusive. Here we generate quiescent Lgr5+ stem cells in vitro by inhibition of the EGF-receptor (EGFR) and mitogen-associated protein kinase (MAPK) signaling pathways in organoids, a state that can be readily reversed. Quiescent Lgr5+ stem cells gain a distinct molecular signature, biased towards EEC differentiation. Indeed, combined inhibition of Wnt, Notch and MAPK pathways efficiently generates a diversity of EEC subtypes in vitro. Our observations uncouple Wnt-dependent stem cell maintenance from EGF-dependent proliferation and cell fate choice, and provide an in vitro approach for the study of the elusive EECs.

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Human colon cancer cell lines: NT(untreated) vs EGF, Cetuximab and Gefitinib treatments

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