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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.

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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.

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RNA Sequencing Analysis of NCAPD2 Knockdown in Lung Adenocarcinoma Cell Line PC9

Project description:This study investigates the effect of NCAPD2 knockdown on lung adenocarcinoma (LUAD) by performing RNA sequencing on PC9 cell lines. The experiment included three control PC9 cells and three PC9 cells in which NCAPD2 was knocked down using shRNA. This RNA sequencing experiment aims to elucidate the role of NCAPD2 in regulating gene expression associated with tumor proliferation, migration, and survival in LUAD. Analysis of differential gene expression provides insights into the pathways affected by NCAPD2 knockdown, with an emphasis on signaling pathways critical to LUAD progression, such as the PI3K/AKT pathway.

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Multiome analysis of PDxOs (HCI-003, HCI-005, HCI-011) treated with a CDK4/6 inhibitor for 3 weeks

Project description:This study uses single-nucleus multiome profiling, as well as bulk methylation profiling, to characterize the transcriptional, chromatin accessibility, and DNA methylation changes after 3 weeks of CDK4/6 inhibitor treatment in organoids grown from patient-derived xenograft tumors (PDxOs) generated from 3 patients: HCI-003, HCI-005, and HCI-011.

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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

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TPX2-mediated autophagy maintains cancer stemness in LUAD

Project description:Targeting protein for Xklp2 (TPX2) is a mitotic regulator frequently overexpressed in lung adenocarcinoma (LUAD), while its role in cancer stemness and autophagy remains incompletely understood. In this study, integrative bioinformatic analyses based on TCGA and GTEx datasets revealed that TPX2 overexpression in LUAD was associated with poor prognosis, elevated stemness scores, and increased expression of cancer stem cell-related markers. To investigate the molecular mechanisms underlying TPX2-mediated regulation in LUAD, RNA sequencing was performed in PC9 cells following TPX2 knockdown. Transcriptomic profiling and pathway analyses identified significant alterations in autophagy-related signaling pathways. In parallel, co-immunoprecipitation coupled with mass spectrometry (IP-MS) was conducted to characterize TPX2-associated protein interactions and explore potential regulatory networks involved in autophagy. Functional experiments further demonstrated that TPX2 depletion impaired autophagic flux and reduced stemness-associated phenotypes in LUAD cells, whereas TPX2 overexpression exerted opposite effects. These data provide transcriptomic and proteomic resources for investigating the role of TPX2-mediated autophagy in LUAD progression and cancer stemness.

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Single-cell RNA sequencing of EGFR/RB1/TP53-mutant LUAD cell lines with and without PHOX2B overexpression to assess neuroendocrine phenotype induction

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N'-(1-phenylethylidene)-benzohydrazide cytotoxicity is LSD1 independent and linked to Fe-S cluster disruption in Ewing sarcoma

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2025-12-04 | GSE286100 | GEO

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

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