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Epigenome analyses reveal histone H4K20me3 and radiation related genes in NSCLC cell

ABSTRACT: Purpose: Radiotherapy is useful for non-small cell lung cancer (NSCLC) patients who cannot be treated surgically. Modification of histone proteins also occurs during radiotherapy, and affects gene expression. In this study, we assessed the effects of radiotherapy on histone H4K20me3 in NSCLC cells. Methods: NCI-H460 NSCLC cell line were subjected to gamma irradiation. To reveal H4K20me3-related genes, we conducted chromatin immunoprecipitation(ChIP) and ChIP-sequencing. Results: We evaluated the H4K20me3-related genes through ChIP-sequencing.

ORGANISM(S): Homo sapiens

PROVIDER: GSE133519 | GEO | 2020/05/12

REPOSITORIES: GEO

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Transcriptome analyses reveal epigenetic and radiation related genes in NSCLC cell

Project description:Purpose: Radiotherapy is useful for non-small cell lung cancer (NSCLC) patients who cannot be treated surgically. Modification of histone proteins occurs during radiotherapy, and affects gene expression.In this study, we assessed the effects of radiotherapy on histone modification via 3-deazaneplanocin A (DZNep) in NSCLC cells. Methods: NCI-H460 NSCLC cell line were subjected to gamma irradiation. To reveal histone modification reagent DZNep targeted genes, we conducted mRNA-sequencing. Results: We evaluated the epigenetic regulation of autophagy-related genes by DZNep through mRNA-sequencing, and we identified genes that are differentially expressed upon irradiation, including a candidate histone modification target gene.

2020-05-12 | GSE133518 | GEO

The HDAC inhibitor panobinostat acts as a sensitizer for erlotinib activity in EGFR mutated and wildtype NSCLC cells

Project description:The receptor tyrosine kinase (RTK) EGFR is overexpressed and mutated in NSCLC. These mutations can be targeted by RTK inhibitors (TKIs), such as erlotinib. Chromatin-modifying agents offer a novel therapy approach by sensitizing tumor cells to TKIs. The NSCLC cell lines HCC827 (EGFR mutant, adenocarcinoma), A549 (EGFR wt, adenocarcinoma) and NCI-H460 (EGFR wt, large cell carcinoma) were analyzed by SNP6.0 array. Changes in proliferation were quantified by WST-1 assay, apoptosis by Annexin V/7-AAD flow cytometry and histone marks (acH3, H3K4me1,-2,-3) by immunoblotting. Expectedly, the EGFR wt cell lines A549 and NCI-H460 were insensitive to the growth-inhibiting effect of single-agent erlotinib (IC50 70-100µM), compared to HCC827 (IC50 <0.02μM). Treatment with panobinostat diminished growth to <50% in both EGFR wt and <30% in HCC827 cells. The combination of both drugs significantly reduced proliferation by ≥70% in A549, >95% in HCC827, but not further in NCI-H460. Panobinostat alone induced differentiation and expression of p21WAF1/CIP1 and p53 in all three cell lines, with almost no further increase when combined with erlotinib. In contrast, combination treatment additively decreased pERK, pAKT and pEGFR in A549, and synergistically induced acH3 in both adenocarcinoma lines. Surprisingly, we also saw an induction of H3K4 methylation marks in all three cell lines. In conclusion, panobinostat synergistically sensitized lung adenocarcinoma cells to the antiproliferative effects of erlotinib. Since single-agent erlotinib has only modest clinical effects in adenocarcinoma EGFR wt patients, combination therapy with an HDACi might offer a promising therapy approach to extend this activity. Copy-number analysis of three NSCLC cell lines HCC827, A549 and NCI-H460 (in unicates) was performed according to protocol by Affymetrix Genome-Wide Human SNP-Array 6.0.

2014-12-03 | E-GEOD-63784 | biostudies-arrayexpress

Epigenome analyses reveal histone H4K20me3 and radiation related genes in NSCLC cell

Project description:Epigenome analyses reveal histone H4K20me3 and radiation related genes in NSCLC cell

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CRISPR screen of radiation resistant genes in NSCLC

Project description:Radiotherapy is an important treatment for non-small cell lung cancer (NSCLC). It not only kills tumor cells directly, but also promotes the efficacy of immunotherapy. However, resistance to radiotherapy is still an unavoidable clinical challenge. In this study, we used radiation-sensitive H460 cell line to stably express Cas9 and CRISPR GeCKO v2 library (A and B). Then a single 4GY irradiation was given, and after the cells resumed proliferation, the total genome was extracted and second-generation sequencing was performed. Genes directly associated with resistance to radiotherapy were identified in comparison to controls without any treatment.

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H4K20me3 co-localizes with activating histone modifications at transcriptionally dynamic regions in embryonic stem cells

Project description:Bivalent chromatin domains consisting of the activating histone 3 lysine 4 trimethylation (H3K4me3) and repressive histone 3 lysine 27 trimethylation (H3K27me3) histone modifications are enriched at developmental genes that are repressed in embryonic stem cells but active during differentiation. However, it is unknown whether another repressive histone modification, histone 4 lysine 20 trimethylation (H4K20me3), co-localizes with activating histone marks in ES cells. Here, we describe the previously uncharacterized coupling of the repressive H4K20me3 heterochromatin mark with the activating histone modifications H3K4me3 and histone 3 lysine 36 trimethylation (H3K36me3), and transcriptional machinery (RNA polymerase II; RNAPII), in ES cells. These newly described bivalent domains consisting of H3K4me3/H4K20me3 are predominantly located in intergenic regions and near transcriptional start sites of active genes, while H3K36me3/H4K20me3 are located in intergenic regions and within gene body regions of active genes. Global sequential ChIP, also termed reChIP-Seq, confirmed the simultaneous presence of H3K4me3 and H4K20me3 at the same genomic regions in ES cells. Genes containing H3K4me3/H4K20me3 exhibit decreased RNAPII pausing and are poised for deactivation of RNAPII binding during differentiation relative to H3K4me3 marked genes. An evaluation of transcription factor (TF) binding motif enrichment revealed that DNA sequence may play a role in shaping the landscape of these novel bivalent domains. Moreover, H3K4me3/H4K20me3 and H3K36me3/H4K20me3 bound regions are enriched with repetitive LINE and LTR elements.

2018-06-18 | GSE115907 | GEO

ChIP-SEQ of H4K20me3 in BCSCsSETD4 and BCSCsGFP

Project description:We report the ChIP-SEQ results of H4K20me3 in BCSCsSETD4 and BCSCsGFP. To explore epigenetic regulation by H4K20me3 in BCSC quiescence, we performed chromatin immunoprecipitation sequencing (ChIP-seq) using BCSCsSETD4 and BCSCsGFP. Quiescent BCSCsSETD4 showed marked enrichment of H4K20me3 modifications relative to BCSCsGFP.

2019-10-25 | GSE123841 | GEO

H4K20me3 methyltransferase SMYD5 controls heterochromatin and chromosome integrity during embryonic stem cell differentiation

Project description:Epigenetic regulation of chromatin states is thought to control gene expression programs during lineage specification. However, the roles of repressive histone modifications such as trimethylated histone lysine 20 (H4K20me3) in development and genome stability are largely unknown. Here, we show that depletion of SMYD5, a H4K20me3 methyltransferase, leads to decreased H4K20me3 and H3K9me3 ChIP-Seq levels, and de-repression of endogenous LTR/LINE elements during differentiation. SMYD5 depletion results in chromosomal aberrations and the formation of transformed cells that exhibit decreased H4K20me3 and H3K9me3 levels and an expression signature consistent with multiple human cancers. Moreover, dysregulated gene expression in SMYD5 cancer cells is associated with LTR/ERV elements and decreased H4K20me3. These findings implicate an important role for SMYD5 in maintaining chromosome integrity by regulating heterochromatin and repressing endogenous repetitive DNA elements during differentiation.

2018-02-13 | GSE94955 | GEO

The HDAC inhibitor panobinostat acts as a sensitizer for erlotinib activity in EGFR mutated and wildtype NSCLC cells

Project description:Background: The receptor tyrosine kinase (RTK) EGFR is overexpressed and mutated in NSCLC. These mutations can be targeted by RTK inhibitors (TKIs) such as erlotinib. Chromatin-modifying agents may offer a novel therapeutic approach by sensitizing tumor cells to TKIs. Methods: The NSCLC cell lines HCC827 (EGFR mutant, adenocarcinoma), A549 (EGFR wt, adenocarcinoma) andNCI-H460 (EGFR wt, large cell carcinoma) were analyzed by SNP6.0 array. Changes in proliferation after panobinostat (LBH-589, PS) and erlotinib treatment were quantified by WST-1 assay and apoptosis by Annexin V/7-AAD flow cytometry. Abundance of target proteins and histone marks (acH3, H3K4me1/2/3) was determined by immunoblotting. Results: As expected, the EGFR wt cell lines A549 and NCI-H460 were quite insensitive to the growth-inhibitory effect of single-agent erlotinib (IC50 70-100 μM), compared to HCC827 (IC50 < 0.02 μM). PS treatment diminished growth to <50 % in both EGFR wt cells, and <30 % in HCC827. The combination of both drugs reduced proliferation by >95 % in HCC827, ≥70 % in A549, but not further in NCI-H460. PS alone induced differentiation and expression of p21WAF1/CIP1 and p53 and decreased CHK1 in all three cell lines, with almost no further effect when combined with erlotinib. In contrast, combination treatment additively decreased pEGFR, pERK, pAKT in A549, and synergistically induced acH3 in both adenocarcinoma lines. Surprisingly, we saw an induction of H3K4 methylation marks after erlotinib treatment in HCC827 (and to a lesser extent in A549) that was even further enhanced by combination with PS. Conclusion: We were able to show that PS synergistically sensitized lung adenocarcinoma cells to the antiproliferative effects of erlotinib. Since single-agent erlotinib has only modest clinical effects in lung adenocarcinoma EGFR wt patients, its combination with an HDACi might offer a promising therapy approach.

2014-12-03 | GSE63784 | GEO

ChIP-Seq data for REST, MCAF1, Ring1b and H4K20me3 in mouse embryonic stem (ES) cells

Project description:Multiple protein complexes and histone marks have been implicated and/or associated with gene repression in ES cells. To gain insights into repressive complexes present at repressed genes and their associated chromatin state, we profiled REST, MCAF1, Ring1b and H4K20me3 in mouse ES cells. DNA was enriched by chromatin immunoprecipitation (ChIP) and analyzed by Solexa sequencing. ChIP was performed using an antibody against REST, MCAF1, Ring1b and H4K20me3.

2011-01-19 | E-GEOD-26680 | biostudies-arrayexpress

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