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Regulation of inducible genes in epithelial to mesenchymal transition by chromatinized PKC-theta

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE53335 | GEO | 2014/06/22

SECONDARY ACCESSION(S): PRJNA231740

REPOSITORIES: GEO

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Regulation of inducible genes in epithelial to mesenchymal transition by chromatinized PKC-theta

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-06-22 | E-GEOD-53335 | biostudies-arrayexpress

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Chromatinized PKC-q directly regulates inducible genes in epithelial to mesenchymal transition and breast cancer stem cells

Project description:Epithelial to mesenchymal transition (EMT) is activated during cancer invasion and metastasis, enriches for cancer stem cells (CSCs), and contributes to therapeutic resistance and disease recurrence. Signal transduction kinases play a pivotal role as chromatin-anchored proteins in eukaryotes. Here we report for the first time that protein kinase C-theta (PKC-q) regulates EMT by acting as a critical chromatin-anchored switch for inducible genes via TGF-β and the key inflammatory regulatory protein, NFkB. Chromatinized PKC-q exists as an active transcription complex and is required to establish a permissive chromatin state at signature EMT genes. Genome-wide analysis identifies a unique cohort of inducible PKC-q-sensitive genes that are directly tethered to PKC-q in the mesenchymal state. Collectively, we show that crosstalk between signaling kinases and chromatin is critical for eliciting inducible transcriptional programs that drive mesenchymal differentiation and CSC formation, providing novel mechanisms to target using epigenetic therapy in breast cancer.

2014-06-22 | GSE53320 | GEO

Chromatinized PKC-q directly regulates inducible genes in epithelial to mesenchymal transition and breast cancer stem cells

Project description:Epithelial to mesenchymal transition (EMT) is activated during cancer invasion and metastasis, enriches for cancer stem cells (CSCs), and contributes to therapeutic resistance and disease recurrence. Signal transduction kinases play a pivotal role as chromatin-anchored proteins in eukaryotes. Here we report for the first time that protein kinase C-theta (PKC-q) regulates EMT by acting as a critical chromatin-anchored switch for inducible genes via TGF-M-NM-2 and the key inflammatory regulatory protein, NFkB. Chromatinized PKC-q exists as an active transcription complex and is required to establish a permissive chromatin state at signature EMT genes. Genome-wide analysis identifies a unique cohort of inducible PKC-q-sensitive genes that are directly tethered to PKC-q in the mesenchymal state. Collectively, we show that crosstalk between signaling kinases and chromatin is critical for eliciting inducible transcriptional programs that drive mesenchymal differentiation and CSC formation, providing novel mechanisms to target using epigenetic therapy in breast cancer. 2 biological samples were analysed, Immunoprecipitated and total input samples were obtained from each biological treatment. 2 Technical replicates were performed (samples from the sample lib prep were run on two different lanes).

2014-06-22 | E-GEOD-53320 | biostudies-arrayexpress

Dynamic Chromatin Modification Sustains Epithelial-Mesenchymal Transition following Inducible Expression of Snail-1

Project description:This SuperSeries is composed of the SubSeries listed below.

2013-12-18 | GSE52593 | GEO

Role of iron in the regulation of the epithelial-to-mesenchymal transition

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-10-01 | GSE121664 | GEO

Epigenetic regulation of epithelial-mesenchymal transition.

Project description:Epithelial-mesenchymal transition (EMT) is an essential process for morphogenesis and organ development which reversibly enables polarized epithelial cells to lose their epithelial characteristics and to acquire mesenchymal properties. It is now evident that the aberrant activation of EMT is also a critical mechanism to endow epithelial cancer cells with migratory and invasive capabilities associated with metastatic competence. This dedifferentiation program is mediated by a small cohort of pleiotropic transcription factors which orchestrate a complex array of epigenetic mechanisms for the wide-spread changes in gene expression. Here, we review major epigenetic mechanisms with an emphasis on histone modifications and discuss their implications in EMT and tumor progression. We also highlight mechanisms underlying transcription regulation concerted by various chromatin-modifying proteins and EMT-inducing transcription factors at different molecular layers. Owing to the reversible nature of epigenetic modifications, a thorough understanding of their functions in EMT will not only provide new insights into our knowledge of cancer progression and metastasis, but also facilitate the development of diagnostic and therapeutic strategies for human malignancy.

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TET1 regulates hypoxia-induced epithelial-mesenchymal transition through DNA demethylation

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-08-01 | E-GEOD-59990 | biostudies-arrayexpress

Architecture of Epigenetic Reprogramming Following Twist1 Mediated Epithelial-Mesenchymal Transition

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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Oncogenic PKC-? activates Vimentin during epithelial-mesenchymal transition in melanoma; a study based on PKC-? and PKC-? specific inhibitors.

Project description:Melanoma is one of the fastest growing cancers in the United States and is accompanied with a poor prognosis owing to tumors being resistant to most therapies. Atypical protein kinase Cs (aPKC) are involved in malignancy in many cancers. We previously reported that aPKCs play a key role in melanoma's cell motility by regulating cell signaling pathways which induce epithelial-mesenchymal Transition (EMT). We tested three novel inhibitors; [4-(5-amino-4-carbamoylimidazol-1-yl)-2,3-dihydroxycyclopentyl] methyl dihydrogen phosphate (ICA-1T) along with its nucleoside analog 5-amino-1-((1R,2S,3S,4R)-2,3-dihydroxy-4-methylcyclopentyl)-1H-imidazole-4-carboxamide (ICA-1S) which are specific to protein kinase C-iota (PKC-?) and 8-hydroxy-1,3,6-naphthalenetrisulfonic acid (?-Stat) which is specific to PKC-zeta (PKC-?) on cell proliferation, apoptosis, migration and invasion of two malignant melanoma cell lines compared to normal melanocytes. Molecular modeling was used to identify potential binding sites for the inhibitors and to predict selectivity. Kinase assay showed >50% inhibition for specified targets beyond 5 ?M for all inhibitors. Both ICA-1 and ?-Stat significantly reduced cell proliferation and induced apoptosis, while ICA-1 also significantly reduced migration and melanoma cell invasion. PKC-? stimulated EMT via TGF?/Par6/RhoA pathway and activated Vimentin by phosphorylation at S39. Both ICA-1 and ?-Stat downregulate TNF-? induced NF-?B translocation to the nucleus there by inducing apoptosis. Results suggest that PKC-? is involved in melanoma malignancy than PKC-?. Inhibitors proved to be effective under in-vitro conditions and need to be tested in-vivo for the validity as effective therapeutics. Overall, results show that aPKCs are essential for melanoma progression and metastasis and that they could be used as effective therapeutic targets for malignant melanoma.

| S-EPMC6363030 | biostudies-literature

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