SOX2 Genomic Localization in Small Cell Lung Cancer Cell Lines
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA757626 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15607000.fastq.gz | Fastqsanger.gz | |||
| SRR15607001.fastq.gz | Fastqsanger.gz | |||
| SRR15607002.fastq.gz | Fastqsanger.gz | |||
| SRR15607003.fastq.gz | Fastqsanger.gz | |||
| SRR15607004.fastq.gz | Fastqsanger.gz |
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Project description:SOX2 is a transcription factor essential for self-renewal and pluripotency of embryonic stem cells. Recently SOX2 was found overexpressed in the majority of the lung squamous cell carcinoma (SQC), in which it acts as a lineage-survival oncogene. However, downstream targets/pathways of SOX2 in lung SQC cells remain to be identified. In order to identify genes/pathways likely to be downstream of SOX2, we conducted SOX2 silencing experiments in LK2 and NCI-H520 (H520 thereafter), two SOX2-abundant lung SQC cell lines and analyzed global gene transcription changes by gene expression microarray assay. Each of H520 and LK2 cell lines was treated with either pooled siRNAs of SOX2 or non-silencing (control) siRNAs. After 48 h, cells were harvested and totoal RNA extracted for gene expression microarray analysis using Illumina HumanHT12 v3 BeadChip.
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Project description:Small-cell lung cancer (SCLC) is an exceptionally aggressive disease with poor prognosis. Here, we obtained exome, transcriptome and copy-number alteration data from approximately 53 samples consisting of 36 primary human SCLC and normal tissue pairs and 17 matched SCLC and lymphoblastoid cell lines. We also obtained data for 4 primary tumors and 23 SCLC cell lines. We identified 22 significantly mutated genes in SCLC, including genes encoding kinases, G protein-coupled receptors and chromatin-modifying proteins. We found that several members of the SOX family of genes were mutated in SCLC. We also found SOX2 amplification in ?27% of the samples. Suppression of SOX2 using shRNAs blocked proliferation of SOX2-amplified SCLC lines. RNA sequencing identified multiple fusion transcripts and a recurrent RLF-MYCL1 fusion. Silencing of MYCL1 in SCLC cell lines that had the RLF-MYCL1 fusion decreased cell proliferation. These data provide an in-depth view of the spectrum of genomic alterations in SCLC and identify several potential targets for therapeutic intervention.
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Project description:Pioneer transcription factors (TFs) such as SOX2 play critical roles in control of stem cell identity and are dysregulated in many human cancers. For example, SOX2 regulates the self-renewal of neural stem cells (NSCs), and is typically highly expressed in glioblastoma stem cells, where it is known to induce an immature NSC-like state. Here, we explored the regulation of SOX2 by phosphorylation during cell division and identify an unexpected role for mitotic SOX2 as an inducer of genomic damage. We find that SOX2 adopts a distinct phosphorylated state in NSCs during mitosis, regulated by the mitotic kinase CDK1. Mapping of SOX2 genome occupancy and chromatin accessibility shows that a subset of SOX2 remains bound to the interphase targets, consistent with mitotic bookmarking, but phosphorylated SOX2 is redistributed to constitutive heterochromatin, including telomeres. Ablation of SOX2 phosphorylation leads to promiscuous chromatin binding across the genome and triggers prolonged mitotic transit times and increased susceptibility to DNA damage. These findings show that excessive levels of SOX2 protein in mitosis trigger inappropriate opening of chromatin and downstream chromosomal damage. Elevated levels of SOX2 in cancers may therefore have dual oncogenic roles: imposing stemness during interphase via their well-known transcriptional roles, but simultaneously inducing genomic damage during mitosis due to their unconstrained pioneer factor activity.
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