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Expression data of LUAD cell line PC9 treated with 2 uM HCI-2509 for 48 hours

ABSTRACT: Expression data of LUAD cell line PC9 treated with 2 uM HCI-2509 for 48 hours

PROVIDER: PRJNA482995 | ENA |

REPOSITORIES: ENA

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Expression data of LUAD cell line PC9 treated with 2 uM HCI-2509 for 48 hours

Project description:The epigenetic regulator LSD1 is overepxpressed in lung adenocarcinoma (LUAD). HCI-2509 a LSD1 inhibitor leads to growth arrest in in vitro tumor models. To identify the underlying molecular mechanims behind LSD1 overexpression, we examined the gene expression patterns using microarray in the LUAD cell line PC9 after HCI-2509 treatment

2018-07-27 | GSE117702 | GEO

Reversible LSD1 Inhibition with HCI-2509 induces the p53 gene expression signature in high-risk neuroblastoma cells

Project description:Lysine-Specific Demethylase 1 (LSD1) over-expression correlates with poorly differentiated neuroblastoma and predicts poor outcome despite multimodal therapy. We have studied the efficacy of reversible and specific LSD1 inhibition with HCI-2509 in neuroblastoma cell lines and particularly the effect of HCI-2509 on the transcriptomic profile in MYCN amplified NGP cells. Cell survival assays show that HCI-2509 is cytotoxic to poorly differentiated neuroblastoma cell lines in low micromole or lower doses. Transcriptional profiling of NGP cells treated with HCI-2509 shows a significant effect on p53, cell cycle, MYCN and hypoxia pathway gene sets. HCI-2509 results in increased histone methyl marks and p53 levels along with cell cycle arrest in the G2/M phase and inhibition of colony formation of NGP cells. Our findings indicate that LSD1 inhibition with HCI-2509 has a multi-target effect in MYCN amplified high-risk neuroblastoma cells.

2019-01-01 | GSE104526 | GEO

Expression data of A549 cells treated with 2 µM of HCI-2509 for 48 h

Project description:Inhibition of LSD1 is a novel option for treatment of lung cancer. Using HCI-2509, a specific inhibitor of LSD1, results in a cell cycle arrest as wel as a shift in global histone 3 lysine 4 and lysine 9 dimethylation pattern. Using microarrays we aim to illucidate the changed transcriptome upon treatement of HCI-2509 in lung adenocarcinoma cell line A549.

2017-08-30 | GSE103256 | GEO

Reversible LSD1 Inhibition with HCI-2509 induces the p53 gene expression signature in high-risk neuroblastoma cells

Project description:Reversible LSD1 Inhibition with HCI-2509 induces the p53 gene expression signature in high-risk neuroblastoma cells

| PRJNA412925 | ENA

Gene expression profiling of drug-tolerant persister PC9 non-small cell lung cancer cells derived from osimertinib treatment

Project description:Targeting drug tolerant persister (DTP) cells may present a therapeutic opportunity to eliminate residual surviving tumor cells and impede relapse. We sought to identify therapeutically exploitable vulnerabilities in DTP cells using the EGFR-mutant non-small cell lung cancer cell line PC9 as an experimental model. Here we provide RNAseq gene expression profiling data generated from parental PC9 cells compared to PC9 DTP cells generated from nine days of treatment with 2 uM osimertinib. These data can be used to identify genes and pathways which are upregulated in DTP cells, revealing potential therapeutic targets.

2020-06-25 | GSE153183 | GEO

Ewing sarcoma resistance to SP-2509 is not mediated through KDM1A/LSD1 mutation I

Project description:The transcriptional profile of A673 parental and SP-2509 Drug resistant cells treated with DMSO and SP-2509 (2uM 48hrs)

2018-12-26 | GSE118864 | GEO

Therapeutic targeting of KDM1A/LSD1 in Ewing sarcoma engages the ER-stress response I

Project description:The purpose of this study was to define biomarkers of sensitivty and mechanisms of resistance to the KDM1A/LSD1 inhibtor SP-2509 (HCI-2509) in Ewing sarcoma cell lines. We report that regardless of drug sensitivity all cell lines engage the UPR and ER-stress response following treatment with SP-2509 resulting in apoptotic cytotoxicity. In addition hypersentsitive cell lines shared a common basal transcriptnomic profile, with hypersensitive cell lines signficantly inducing ETS1 which was not observed in sensitive cell lines.

2019-05-03 | GSE98785 | GEO

Gene expression of PC9 and PC9-OR cell line [JXQ_RNA]

Project description:To investigate the abnormal gene expression in Osimertinib Resistance lung cancer cell line, We performed gene expression profiling analysis using data obtained from RNA-seq of PC9 cell line and PC9-OR cell line.

2024-03-13 | GSE222820 | GEO

Transcriptome analysis of PC9 cells with gefitinib or/and hypoxia treatment and comparison with gefitinib resistant PC9 cells and ALDH positive PC9 cells

Project description:Inevitable gefitinib resistance and relapse of the disease was the biggest hurdle to NSCLC treatment. Importantly, the role of hypoxia in solid tumor tissues in vivo in gefitinib acquired resistance and its relationship to lung cancer stem cells (LCSCs) has not been fully elucidated. Here, the PC9 cells were treated with short term gefitinib or/and hypoxia, also, PC9 gefitnib resistant (PC9-GR) cell line was established and ALDH positive PC9 cells were sorted by FACs. Transcriptome analysis among those PC9 cell groups revealed the important role of hypoxia in gefitinib acquired resistance and signaling transduction change, which may critical for NSCLC disease progression and recurrence.

2017-10-31 | GSE69599 | GEO

Characterization of a novel hormone-responsive endometrial cancer cell line: HCI-EC-23 [RNA-seq]

Project description:Most endometrial cancers are driven by excess estrogen signaling and express the hormone receptor estrogen receptor alpha (ER). Evaluation of the estrogen response in endometrial cancer cells has been limited by the availability of hormonally responsive in vitro models, with one cell line, Ishikawa, being used in most studies. Here, we describe a novel, adherent endometrioid endometrial cancer (EEC) cell line model, HCI-EC-23. We show that HCI-EC-23 retains ER expression and that ER functionally responds to 17b-estradiol (E2) induction over a range of passages. We also demonstrate that this cell line retains paradoxical activation of ER by tamoxifen, which is also observed in Ishikawa and is consistent with clinical data. The mutational landscape shows that HCI-EC-23 is mutated at many of the commonly altered genes in EEC, has relatively few copy-number alterations, and is microsatellite instable high (MSI-high). In vitro proliferation of HCI-EC-23 is modestly enhanced by E2 but is strongly reduced upon combination E2 and progesterone (P4) treatment. HCI-EC-23 exhibit strong E2 dependence for tumor growth in vivo and tumor size is reduced by combination E2 + P4 treatment. Molecular characterization of E2 induction in HCI-EC-23 revealed hundreds of estrogen-responsive genes that significantly overlapped with those regulated in Ishikawa. Analysis of ER genome binding identified similar patterns in HCI-EC-23 and Ishikawa, although ER exhibited more bound sites in Ishikawa. This study demonstrates that HCI-EC-23 is estrogen-responsive and can be used to study the hormonal aspects of endometrial cancer.

2022-08-02 | GSE210123 | GEO

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