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Neuroendocrine lineage commitment of small cell lung cancers can be leveraged into p53-independent non-cytotoxic therapy [CUT&Tag]

ABSTRACT: Neuroendocrine lineage commitment of small cell lung cancers can be leveraged into p53-independent non-cytotoxic therapy [CUT&Tag]

PROVIDER: PRJNA997358 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25387718_1.fastq.gz	Fastqsanger.gz
	SRR25387718_2.fastq.gz	Fastqsanger.gz
	SRR25387719_1.fastq.gz	Fastqsanger.gz
	SRR25387719_2.fastq.gz	Fastqsanger.gz
	SRR25387720_1.fastq.gz	Fastqsanger.gz

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Neuroendocrine lineage commitment of small cell lung cancers can be leveraged into p53-independent non-cytotoxic therapy [CUT&Tag]

Project description:Small cell lung cancers (SCLC) rapidly resist cytotoxic chemotherapy and immune-checkpoint inhibitor (ICI) treatments. New, non-cross-resistant therapies are thus needed. SCLC cells are committed into neuroendocrine-lineage then maturation-arrested. The corepressor DNA methyltransferase 1 (DNMT1) mediates the maturation-arrests: (i) the repression mark methylated-CpG, written by DNMT1, is retained at suppressed neuroendocrine-lineage genes, even as other repression marks are erased; (ii) DNMT1 is recurrently amplified, while Ten-Eleven-Translocation 2 (TET2) that functionally opposes DNMT1 is deleted; (iii) DNMT1 is recruited into neuroendocrine-lineage master transcription factor (ASCL1, NEUROD1) hubs in SCLC cells; and (iv) DNMT1 knock-down activated ASCL1-target genes and released SCLC cell cycling exits by terminal lineage-maturation, cycling exits that do not require the p53/apoptosis-pathway used by cytotoxic chemotherapy. Inhibiting DNMT1/corepressors with clinical compounds accordingly extended survival of mice with chemo- and ICI-refractory disseminated SCLC. Neuroendocrine-lineage commitment of SCLC cells can thus be leveraged into p53/apoptosis-independent therapy, active against chemo- and ICI-refractory SCLC.

2023-07-25 | GSE238003 | GEO

Neuroendocrine lineage commitment of small cell lung cancers can be leveraged into p53-independent non-cytotoxic therapy [RNA-seq]

2023-07-25 | GSE238006 | GEO

Neuroendocrine lineage commitment of small cell lung cancers can be leveraged into p53-independent non-cytotoxic therapy

Project description:Neuroendocrine lineage commitment of small cell lung cancers can be leveraged into p53-independent non-cytotoxic therapy

| PRJNA997363 | ENA

Neuroendocrine lineage commitment of small cell lung cancers can be leveraged into p53-independent non-cytotoxic therapy [RNA-seq]

Project description:Neuroendocrine lineage commitment of small cell lung cancers can be leveraged into p53-independent non-cytotoxic therapy [RNA-seq]

| PRJNA997364 | ENA

Neuroendocrine lineage commitment of small cell lung cancers can be leveraged into p53-independent non-cytotoxic therapy.

Project description:Small cell lung cancers (SCLCs) rapidly resist cytotoxic chemotherapy and immune checkpoint inhibitor (ICI) treatments. New, non-cross-resistant therapies are thus needed. SCLC cells are committed into neuroendocrine lineage then maturation arrested. Implicating DNA methyltransferase 1 (DNMT1) in the maturation arrests, we find (1) the repression mark methylated CpG, written by DNMT1, is retained at suppressed neuroendocrine-lineage genes, even as other repression marks are erased; (2) DNMT1 is recurrently amplified, whereas Ten-Eleven-Translocation 2 (TET2), which functionally opposes DNMT1, is deleted; (3) DNMT1 is recruited into neuroendocrine-lineage master transcription factor (ASCL1, NEUROD1) hubs in SCLC cells; and (4) DNMT1 knockdown activated ASCL1-target genes and released SCLC cell-cycling exits by terminal lineage maturation, which are cycling exits that do not require the p53/apoptosis pathway used by cytotoxic chemotherapy. Inhibiting DNMT1/corepressors with clinical compounds accordingly extended survival of mice with chemorefractory and ICI-refractory, p53-null, disseminated SCLC. Lineage commitment of SCLC cells can hence be leveraged into non-cytotoxic therapy able to treat chemo/ICI-refractory SCLC.

| S-EPMC10528072 | biostudies-literature

Neuroendocrine lineage commitment of small cell lung cancers can be leveraged into p53-independent non-cytotoxic therapy

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-07-25 | GSE238007 | GEO

Project description:Neuroendocrine lineage commitment of small cell lung cancers can be leveraged into p53-independent non-cytotoxic therapy

| PRJNA996186 | ENA

Project description:Neuroendocrine lineage commitment of small cell lung cancers can be leveraged into p53-independent non-cytotoxic therapy

| PRJNA996198 | ENA

Transcription factor network dynamics during the commitment to oncogene-induced senescence [CUT&Tag]

Project description:Aberrant oncogenic signaling causes cells to transition into oncogene-induced senescence (OIS) to limit uncontrolled proliferation. Despite being a potent tumor suppressor mechanism, OIS is an unstable cell state susceptible to reprogramming that can promote tumorigenesis. Therefore, elucidating the underlying gene regulatory mechanisms that commit cells to OIS is critical to identifying actionable targets to modulate the senescence state. We previously showed that timely execution of the OIS program is governed by hierarchical transcription factor (TF) networks. However, the gene regulatory mechanisms that prime cells to commit to the OIS fate early upon oncogene hyperactivation are currently not known. Here, we leveraged our time-resolved multi-omic profiling approach to generate TF networks during the first 24 h of oncogenic HRASG12V activation. Using this approach, we demonstrate that the commitment to OIS requires the rearrangement of the TF network on a pre-established epigenomic landscape, priming the cells for the substantial chromatin remodeling that underpins the transition to OIS. Our results provide a detailed map of the chromatin landscape before cells transition to OIS thus offering a platform for manipulation of senescence outcomes of potentially therapeutic value.

2024-07-22 | GSE271460 | GEO

ASCL1 is a lineage oncogene providing therapeutic targets for high-grade neuroendocrine lung cancers

Project description:ChIP-Seq analysis performed on 5 ASCL1(+) cell lines and 2 ASCL1 (-) cell lines in order to understand the transcriptome of ASCL1 as it pertains to high-grade neuroendocrine lung cancers 5 ASCL1(+) lung cancer cell lines and 2 ASCL1(-) lung cancer cell lines were compared using ChIP-Seq analysis

2014-10-01 | E-GEOD-61197 | biostudies-arrayexpress

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