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Effect of restoring endogenous ZFP36L1 expression in CORL47 SCLC Cells that are CRISPR activated for ZFP36L1 (sgZFP36L1-1 and sgZFP36L1-2) or a non-targeting sgRNA (sgControl)

ABSTRACT: To investigate the impact of restoring endogenous ZFP36L1 expression in CORL47 SCLC Cells on neuroendocrine cell state We performed RNA-sequencing on CORL47 SCLC Cells that are CRISPR activated for ZFP36L1 (sgZFP36L1-1 and sgZFP36L1-2) or a non-targeting sgRNA (sgControl)

ORGANISM(S): Homo sapiens

PROVIDER: GSE202114 | GEO | 2022/05/06

REPOSITORIES: GEO

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Effect of restoring endogenous ZFP36L1 expression in CORL47 SCLC Cells that are CRISPR activated for ZFP36L1 (sgZFP36L1-1 and sgZFP36L1-2) or a non-targeting sgRNA (sgControl)

Project description:Effect of restoring endogenous ZFP36L1 expression in CORL47 SCLC Cells that are CRISPR activated for ZFP36L1 (sgZFP36L1-1 and sgZFP36L1-2) or a non-targeting sgRNA (sgControl)

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Effect of LSD1 Inhibitor ORY-1001 on NCI-H1876 small cell lung cancer cells that are CRISPR-inactivated for ZFP36L1 (sgZFP36L1) or ZFP36L1-WT (sgControl)

Project description:To investigate the impact of inactivating ZFP36L1 on the transcriptional response to the LSD1 inhibitor ORY-1001 We performed RNA-sequencing on NCI-H1876 sgZFP36L1 or sgControl cells treated with ORY-1001 or DMSO

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ZFP36L1

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SCLC LCNEC FFPE LMD

Project description:Small-cell lung carcinoma (SCLC) and large-cell neuroendocrine lung carcinoma (LCNEC) are high-grade lung neuroendocrine tumors (NET). However, comparative protein expression within SCLC and LCNEC remains unclear. Here, protein expression profiles were obtained via mass spectrometry-based proteomic analysis.

2019-05-14 | PXD013583 | JPOST Repository

PM01183 and Cisplatin on SCLC cell lines

Project description:Small Cell Lung Cancer (SCLC) is an aggressive neuroendocrine malignancy with a poor prognosis. Here, we focus on the neuroendocrine SCLC subtypes SCLC-A and SCLC-N, whose transcription addiction was driven by ASCL1 and NEUROD1 transcription factors which target E-box motifs to activate up to 40% of total genes, the promoters of which are maintained in a steadily open chromatin environment according to ATAC and H3K27Ac signatures. This leverage is used by the marine agent lurbinectedin, which preferentially targets the CpG islands located downstream of the transcription start site, thus arresting elongating RNAPII and promoting its degradation. This abrogates the expression of ASCL1 and NEUROD1 and of their dependent genes such as BCL2, INSM1, MYC and AURKA, which are responsible for relevant SCLC tumorigenic properties such as inhibition of apoptosis and cell survival, as well as for a part of its neuroendocrine features. In summary, we show how the transcription addiction of these cells becomes their Achilles' heel, and how this is effectively exploited by lurbinectedin as a novel and highly specific SCLC therapeutic endeavor.

2022-02-03 | GSE195663 | GEO

Crebbp loss drives small cell lung cancer and increases sensitivity to HDAC inhibition [SCLC]

Project description:This study assessed tumor suppressor roles of CREBBP in SCLC and other neuroendocrine tumors. Genetically engineered mouse models were used to determine the tumor suppressor role of Crebbp in SCLC and other neuroendocrine tumors.

2018-10-17 | GSE117547 | GEO

A PKA/PP2A AXIS DRIVES THE GROWTH OF NEUROENDOCRINE SCLC

Project description:Small cell lung cancer (SCLC) is an aggressive subtype of lung cancer whose biology is still poorly understood. Using a multiplexed inhibitor beads assay, we identified active kinases in SCLC. Among those, we found that PKA is critical for the expansion of SCLC in culture and in vivo. PKA promotes the neuroendocrine epithelial state associated with SCLC tumor-initiating cells. Phosphoproteomics analyses identify ~200 PKA substrates and show that PKA controls multiple facets of SCLC growth. Notably, the PP2A phosphatase counteracts the oncogenic effects of PKA, and PP2A activators inhibit SCLC as single agents and with chemotherapy. Our data uncover key signaling networks in SCLC and indicate that targeting the PKA/PP2A pathway may help inhibit this lethal neuroendocrine cancer.

2020-02-11 | GSE126353 | GEO

EIF6 conditions drug-tolerant persister-like transdifferentiation in small cell lung carcinoma (SCLC cell lines)

Project description:Drug-tolerant persister cells withstand treatments by adapting their identity through lineage-dependent plasticity during systemic anti-cancer therapies. This phenomenon is evident in small-cell lung carcinoma (SCLC), a lethal neuroendocrine cancer initially responsive (60-80%) to platinum-based chemotherapy but succumbing to resistance within 6 months in advanced stages. This resistance associates with the transdifferentiation of residual tumour cells into a non-neuroendocrine state, a process intricately tied to SCLC's chemotolerance, yet molecular mechanisms governing this lineage conversion remain completed understood. Here we use paired cytoplasmic RNA-seq and polysomal RNA-seq to compare gene expression between NE and non-NE SCLC cell lines on both transcriptional and translational level. We report that first-line chemotherapy induces translation initiation factor eIF6 in drug-tolerant persister-like cells in SCLC, correlating with the non-neuroendocrine state in SCLC. Intervening eIF6 inhibits non-neuroendocrine transdifferentiation, thus enhancing SCLC responsiveness to chemotherapy. This study sheds light on eIF6's potential therapeutic interventions to mitigate treatment resistance in SCLC.

2024-04-30 | GSE262593 | GEO

Response of SCLC to mutant KRAS or EGFR induction

Project description:Lineage transformation between lung cancer subtypes is a poorly understood phenomenon associated with resistance to treatment and poor patient outcomes. Here, we aimed to model this transition in order to define underlying biological mechanisms and identify potential avenues for therapeutic intervention. Small cell lung cancer (SCLC) is neuroendocrine in origin and, in contrast to non-SCLC (NSCLC), rarely contains mutations that drive the MAPK pathway. Likewise, NSCLCs that transform to SCLC concomitantly with development of therapy resistance downregulate MAPK signaling, suggesting an inverse relationship between pathway activation and lineage state. To test this, we activated MAPK in SCLC through conditional expression of mutant KRAS or EGFR, which revealed suppression of the neuroendocrine differentiation program via ERK. We found that ERK induces the expression of ETS factors, phenocopying ERK-mediated effects on transformation into the NSCLC-like phenotype. ATAC-seq demonstrated ERK-driven changes in chromatin accessibility at putative regulatory regions and global chromatin rewiring at neuroendocrine and ETS transcriptional targets. Further, induction of ETS factors as well as suppression of neuroendocrine differentiation were dependent on histone acetyltransferase activities of CBP/p300. Overall, we describe how the ERK-CBP/p300-ETS axis promotes a lineage shift between neuroendocrine and non-neuroendocrine lung cancer phenotypes and provide rationale for the disruption of this program during transformation-driven resistance to targeted therapy.

2021-08-17 | GSE160482 | GEO

Quantitative Proteomics Analysis of Extracellular Vesicles from mouse-derived SCLC cell lines

Project description:Small Cell Lung Cancer (SCLC) tumors are made up of distinct cell subpopulations, including neuroendocrine (NE) and non-NE cells. Proteomic analysis of purified small extracellular vesicles (EV) from these two cell populations were conducted.

2023-11-01 | PXD042153 | Pride

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