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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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H3K9K14ac ChIP-chip in lung cancer cells treated with histone deacetylase inhibitor

ABSTRACT: Lung cancer is the leading cause of cancer mortality worldwide, yet the therapeutic strategy for advanced non-small cell lung cancer (NSCLC) is limitedly effective. In addition, validated histone deacetylase (HDAC) inhibitors for the treatment of solid tumors remain to be developed. Here, we propose a novel HDAC inhibitor, OSU-HDAC-44, as a chemotherapeutic drug for NSCLC. OSU-HDAC-44 was a pan-HDAC inhibitor and exhibits 3-4 times more effectiveness than suberoylanilide hydroxamic acid (SAHA) in suppressing cell viability in various NSCLC cell lines. Upon OSU-HDAC-44 treatment, mitosis and cytokinesis were inhibited and subsequently led to mitochondria-mediated apoptosis. The cytokinesis inhibition resulted from OSU-HDAC-44-mediated degradation of mitosis and cytokinesis regulators Auroroa B and survivin. The deregulation of F-actin dynamics induced by OSU-HDAC-44 was associated with reduction in RhoA activity resulting from srGAP1 induction. Chromatin-immunoprecipitation-on-chip analysis revealed that OSU-HDAC-44 induced chromatin loosening and facilitated transcription of genes involved in crucial signaling pathways such as apoptosis, axon guidance and protein ubiquitination. Finally, OSU-HDAC-44 efficiently inhibited A549 xenograft tumor growth and induced acetylation of histone and non-histone proteins and apoptosis in vivo. Collectively, our data provide compelling evidence that OSU-HDAC-44 is a potent HDAC targeted inhibitor and can be tested for NSCLC chemotherapy. ChIP-chip analysis for H3K9K14ac in A549, H1299 and CL1-1 lung cancer cells treated with 2.5 uM histone deacetylase inhibitor, OSU-HDAC-44, for 2 hours.

ORGANISM(S): Homo sapiens

SUBMITTER: Yi-Ching Wang

PROVIDER: E-GEOD-20304 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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H3K9K14ac ChIP-chip in lung cancer cells treated with histone deacetylase inhibitor

Project description:Lung cancer is the leading cause of cancer mortality worldwide, yet the therapeutic strategy for advanced non-small cell lung cancer (NSCLC) is limitedly effective. In addition, validated histone deacetylase (HDAC) inhibitors for the treatment of solid tumors remain to be developed. Here, we propose a novel HDAC inhibitor, OSU-HDAC-44, as a chemotherapeutic drug for NSCLC. OSU-HDAC-44 was a pan-HDAC inhibitor and exhibits 3-4 times more effectiveness than suberoylanilide hydroxamic acid (SAHA) in suppressing cell viability in various NSCLC cell lines. Upon OSU-HDAC-44 treatment, mitosis and cytokinesis were inhibited and subsequently led to mitochondria-mediated apoptosis. The cytokinesis inhibition resulted from OSU-HDAC-44-mediated degradation of mitosis and cytokinesis regulators Auroroa B and survivin. The deregulation of F-actin dynamics induced by OSU-HDAC-44 was associated with reduction in RhoA activity resulting from srGAP1 induction. Chromatin-immunoprecipitation-on-chip analysis revealed that OSU-HDAC-44 induced chromatin loosening and facilitated transcription of genes involved in crucial signaling pathways such as apoptosis, axon guidance and protein ubiquitination. Finally, OSU-HDAC-44 efficiently inhibited A549 xenograft tumor growth and induced acetylation of histone and non-histone proteins and apoptosis in vivo. Collectively, our data provide compelling evidence that OSU-HDAC-44 is a potent HDAC targeted inhibitor and can be tested for NSCLC chemotherapy.

2010-12-22 | GSE20304 | GEO

Transcription profiling of human

Project description:This SuperSeries is composed of the following subset Series:; GSE9974: The effect of the HDAC inhibitor OSU-HDAC42 on gene expression in esophageal tissues and adenocarcinoma cells I; GSE9976: The effect of the HDAC inhibitor OSU-HDAC42 on gene expression in esophageal tissues and adenocarcinoma cells II Experiment Overall Design: Refer to individual Series

2008-04-05 | E-GEOD-9987 | biostudies-arrayexpress

Transcription profiling of human SEG1 esophageal cell line treated with OSU-HDAC42, time series

Project description:Title: In vitro and in vivo effects of the orally bioavailable phenylbutyrate-derived histone deacetylase inhibitor OSU-HDAC42 on gene expression in esophageal tissues and in esophageal adenocarcinoma cells; Histone deacetylases (HDACs) modulate nucleosomal packaging of DNA, thereby influencing gene transcription and multiple cancer-associated processes. Thus, we conducted microarray analysis at multiple time-points to assess the ability of OSU-HDAC42, the S enantiomer of the previously published compound HDAC-42, to modulate key acid-induced changes as well as to impact other genes altered as the normal esophageal epithelium progresses along the metaplasia-dysplasia-esophageal adenocarcinoma continuum. Experiment Overall Design: SEG-1 cells were pretreated for 24 hours with vehicle or OSU-HDAC42, pulsed with acidified media (pH 3.5; 20 mins at 37C), replenished with media or OSU-HDAC42, and harvested 3, 6 and 24 hours later. Global gene expression analysis was conducted using the human genome chip U133 2.0 Plus.

2008-04-05 | E-GEOD-9974 | biostudies-arrayexpress

Transcription profiling of rat esophageal tissues AND esophageal adenocarcinoma cells treated WITH phenylbutyrate-derived histone deacetylase inhibitor (OSU-HDAC42) OR vehicle TO assess target effect IN an IN vivo MODEL utilized FOR EAC development

Project description:Title: In vitro and in vivo effects of the orally bioavailable phenylbutyrate-derived histone deacetylase inhibitor OSU-HDAC42 on gene expression in esophageal tissues and in esophageal adenocarcinoma cells. Histone deacetylases (HDACs) modulate nucleosomal packaging of DNA, thereby influencing gene transcription and multiple cancer-associated processes. We conducted microarray analysis on esophageal tissue from male Sprague-Dawley rats treated with OSU-HDAC42 or vehicle to assess target effect in an in vivo model utilized for EAC development. Experiment Overall Design: 5-6 week old male Sprague-Dawley rats were administered OSU-HDAC42 (50 mg/kg/dose thrice weekly for a total dose of 350 mg/kg) or vehicle by gavage. Twenty-four hours after the final gavage, the esophagi were harvested and total RNA was isolated using the RNA Mini Kit (Qiagen). Global gene expression analysis was conducted using the 230 2.0 chip (Affymetrix).

2008-04-05 | E-GEOD-9976 | biostudies-arrayexpress

TAG-TMTpro, a hyperplexing quantitative approach for high-throughput proteomic studies

Project description:Isobaric labeling is the most widely used multiplexing quantitative approach in proteomic studies, enabling the comparison of up to 18 samples in a single MS analysis. Expanding the multiplexing capacity is of great necessity for high-throughput proteomic studies. Herein, we establish a novel TAG-TMTpro approach by introducing Ala or Gly residues to peptides prior to TMTpro labeling, which is able to triple the quantitative capacity of TMTpro. We systematically evaluated the Boc-Ala-OSu and Boc-Gly-OSu reaction and optimized the conditions for labeling, side-product elimination and Boc deprotection. We validated the identification and quantification performance using E. coli and HeLa cell lysates. We demonstrated that the TAG-TMTpro approach resulted in good identification reproducibility and reliable quantitative accuracy. The TAG-TMTpro is able to triple the multiplexing capacity of TMTpro reagents, and is a versatile quantitative approach for high-throughput proteomic studies.

2022-10-14 | PXD033711 | Pride

CRTAC1 Enhances the Chemosensitivity of Non-Small Cell Lung Cancer to Cisplatin by Eliciting RyR-mediated Calcium Release and Inhibiting Akt1 Expression

Project description:Sensitivity to platinum-based combination chemotherapy is associated with a favorable prognosis in the patients of non-small cell lung cancer (NSCLC). Here, our results obtained from analyses of the Gene Expression Omnibus database of NSCLC patients showed that cartilage acidic protein 1 (CRTAC1) plays a role in the response to platinum-based chemotherapy. Overexpression of CRTAC1 increased sensitivity to cisplatin in vitro, whereas knockdown of CRTAC1 decreased chemosensitivity of NSCLC cells. In vivo mouse experiments showed that CRTAC1 overexpression increased the antitumor effects of cisplatin. CRTAC1 overexpression promoted NFAT transcriptional activation by increasing intracellular Ca2+ levels, thereby inducing its regulated STUB1 mRNA transcription and protein expression, accelerating Akt1 protein degradation, and in turn enhancing cisplatin-induced apoptosis. Taken together, the present results indicate that CRTAC1 overexpression increases the chemosensitivity of NSCLC to cisplatin treatment by inducing Ca2+-dependent Akt1 degradation and apoptosis, suggesting the potential of CRTAC1 as a biomarker for predicting cisplatin chemosensitivity. Our results further reveal that modulating the expression of CRTAC1 could be a new strategy for increasing the efficacy of cisplatin in chemotherapy of NSCLC patients.

2023-08-29 | PXD041782 | Pride

Expression data from the dorsal and lateral lobes of the prostates of TRAMP mice treated with OSU-CG5

Project description:Cells undergoing malignant transformation often shift their cellular metabolism from primarily oxidative phosphorylation to aerobic glycolysis (the Warburg effect). Energy restriction-mimetic agents (ERMAs), such as 2-deoxyglucose and resveratrol, that target this shift in cellular metabolism have been effective in inhibiting cancer cell growth in vitro, and xenograft tumor growth in vivo. We recently developed a novel ERMA, OSU-CG5, that exhibits higher in vivo activity than previously described ERMAs. In this study, we investigated the effect of OSU-CG5 on global gene expression in the dorsal and lateral lobes of the prostate of transgenic adenocarcinoma of the mouse prostate (TRAMP) mice, and on its ability to suppress lesion progression in these mice. Intact male TRAMP mice were randomized into 2 groups and treated for 4-weeks (from age 6 to 10 weeks) with a vehicle or 100 mg/kg/day OSU-CG5 via oral gavage. At the end of the study, the urogenital tracts were collected and prostates microdissected. RNA was extracted from the dorsal and lateral lobes of the prostates from 3 mice per group, and Affymetrix microarrays were performed.

2013-01-06 | E-GEOD-32422 | biostudies-arrayexpress

The effect of the HDAC inhibitor OSU-HDAC42 on gene expression in esophageal tissues and adenocarcinoma cells I

Project description:Title: In vitro and in vivo effects of the orally bioavailable phenylbutyrate-derived histone deacetylase inhibitor OSU-HDAC42 on gene expression in esophageal tissues and in esophageal adenocarcinoma cells Histone deacetylases (HDACs) modulate nucleosomal packaging of DNA, thereby influencing gene transcription and multiple cancer-associated processes. Thus, we conducted microarray analysis at multiple time-points to assess the ability of OSU-HDAC42, the S enantiomer of the previously published compound HDAC-42, to modulate key acid-induced changes as well as to impact other genes altered as the normal esophageal epithelium progresses along the metaplasia-dysplasia-esophageal adenocarcinoma continuum. Keywords: acid-pulsed cells pretreated with OSU-HDAC42 or vehicle

2008-03-20 | GSE9974 | GEO

Transcription profiling of human HDAC-42 SEG-1 esophageal adenocarcinoma cells

Project description:The role of acid and bile salts in the pathogenesis of esophageal carcinoma arising from Barrett's metaplasia has been well established. Cell proliferation of Barrett's epithelium in response to pulsatile acid exposure has since been confirmed in vivo using endoscopy specimens. Histone deactylases (HDACs) modulate nucleosomal packaging of DNA, thereby influencing gene transcription and multiple cancer-associated processes. Thus, we conducted microarray analysis to assess the ability of HDAC-42 to modulate key acid-induced changes as well as to impact other genes altered as the normal esophageal epithelium progresses along the metaplasia-dysplasia-esophageal adenocarcinoma continuum. Experiment Overall Design: SEG-1 cells were pretreated for 24 hours with vehicle or HDAC-42, pulsed with media or acidified media (pH 3.5; 20 mins at 37C), replenished with media or HDAC-42, and harvested 6 hours later. Global gene expression analysis was conducted using the human genome chip U133 2.0 Plus.

2008-06-15 | E-GEOD-7964 | biostudies-arrayexpress

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Project description:Metastasis is a major cause leading to mortality for lung cancer patients. We identified YWHAZ as a potential metastasis-promoting candidate and found that overexpression of YWHAZ promotes lung cancer cell proliferation, anchorage-independent growth, migration, and invasion in vitro, as well as tumorigenesis and metastasis in vivo. It not only increases cell protrusions and branchings but also induces epithelial-mesenchymal transition. Most importantly, YWHAZ protein could prevent Â£]-catenin from ubiquitination via its association with Â£]-catenin and enhance slug transcriptional activity which is regulated by Â£]-catenin/TCF signaling pathway. Moreover, YWHAZ expression was higher in tumors than in adjacent normal tissues in 63 Non-small-cell lung cancer (NSCLC) patients. NSCLC patients with high YWHAZ expressing tumors had shorter overall survival than those with low-expressing tumors. We conclude that YWHAZ play a critical role in promoting NSCLC metastasis. In this investigation, we used a lung cancer invasion cell model to identify the genes involved in cancer progression. YWHAZ is a potential oncogene whose expression is correlated to the survival of patients with breast, prostate and liver cancers. However, the role of YWHAZ in lung caner progression has not been reported, particularly in metastasis. Here, YWHAZ was ectopically expressed in lower invasive lung cancer cell line its impact on colonogenesis, migration and invasiveness was assessed. The underlying mechanism was explored by YWHAZ-expressed transfectants and microarrays and the clinical relevance was evaluated by quantitative RT-PCR.

2012-11-07 | E-GEOD-20318 | biostudies-arrayexpress

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