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Elevating SOX2 downregulates MYC through a SOX2:MYC signaling axis and induces a slowly cycling proliferative state in human tumor cells

ABSTRACT: Elevating SOX2 downregulates MYC through a SOX2:MYC signaling axis and induces a slowly cycling proliferative state in human tumor cells

PROVIDER: PRJNA788955 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17260160_1.fastq.gz	Fastqsanger.gz
	SRR17260160_2.fastq.gz	Fastqsanger.gz
	SRR17260161_1.fastq.gz	Fastqsanger.gz
	SRR17260161_2.fastq.gz	Fastqsanger.gz
	SRR17260162_1.fastq.gz	Fastqsanger.gz

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Elevating SOX2 downregulates MYC through a SOX2:MYC signaling axis and induces a slowly cycling proliferative state in human tumor cells

Project description:Quiescent/slowly circling tumor cells present a clinical challenge due to their ability to evade treatement. Recent studies have demonstrated that quiescent/slow circling tumor cells hijack embryonic growth arrest mechanisms and consequently resist chemotherapy. Significantly, earlier studies established that high levels of SOX2 in both fetal and tumor cells restrict cell proliferation and induce a slowly cycling state. However, the mechanisms through which elevated SOX2 levels inhibit tumor cell proliferation have not been identified. To identify common mechanisms through which SOX2 elevation restricts tumor cell proliferation, we performed RNA-seq using ONS76 medulloblastoma and LNCaP prostate tumor cells engineered to express SOX2 from an inducible promoter. SOX2 elevation in both cell lines significantly downregulated MYC target genes. Consistent with these findings, elevating SOX2 in five cell lines representing three different human cancer types decreases MYC mRNA and protein levels. Importantly, the expression of a dominant-negative MYC variant, omomyc, recapitulated many of the effects of SOX2 on proliferation, cell cycle, and gene expression. As predicted by our Gene Ontology analysis, elevating SOX2 decreases biosynthetic activity, in particular protein translation. We also demonstrate that rescuing MYC activity in the context of elevated SOX2 induces cell death, indicating that the downregulation of MYC is a critical mechanistic step necessary to maintain survival in the slowly cycling state induced by elevated SOX2. Altogether, our findings uncover a novel SOX2: MYC signaling axis and provide novel insights into the molecular mechanisms through which SOX2 elevation induces a slowly cycling proliferative state.

2022-08-03 | GSE190936 | GEO

Elevating SOX2 Downregulates MYC through a SOX2:MYC Signaling Axis and Induces a Slowly Cycling Proliferative State in Human Tumor Cells.

Project description:Slowly cycling/infrequently proliferating tumor cells present a clinical challenge due to their ability to evade treatment. Previous studies established that high levels of SOX2 in both fetal and tumor cells restrict cell proliferation and induce a slowly cycling state. However, the mechanisms through which elevated SOX2 levels inhibit tumor cell proliferation have not been identified. To identify common mechanisms through which SOX2 elevation restricts tumor cell proliferation, we initially performed RNA-seq using two diverse tumor cell types. SOX2 elevation in both cell types downregulated MYC target genes. Consistent with these findings, elevating SOX2 in five cell lines representing three different human cancer types decreased MYC expression. Importantly, the expression of a dominant-negative MYC variant, omomyc, recapitulated many of the effects of SOX2 on proliferation, cell cycle, gene expression, and biosynthetic activity. We also demonstrated that rescuing MYC activity in the context of elevated SOX2 induces cell death, indicating that the downregulation of MYC is a critical mechanistic step necessary to maintain survival in the slowly cycling state induced by elevated SOX2. Altogether, our findings uncover a novel SOX2:MYC signaling axis and provide important insights into the molecular mechanisms through which SOX2 elevation induces a slowly cycling proliferative state.

| S-EPMC9025961 | biostudies-literature

c-Myc Transcriptionally Amplifies Sox2 Target Genes to Regulate Self-Renewal in Multipotent Otic Progenitor Cells [ChIP-Seq]

Project description:An immortalized multipotent otic progenitor (iMOP) cell was generated by transient expression of c-Myc in Sox2-expressing otic progenitor cells. The procedure activated endogenous c-Myc expression in the cells and amplified existing Sox2-dependent transcripts to promote self-renewal. Downregulation of c-Myc expression following growth factor withdrawal resulted in a molecular switch from self-renewal to otic differentiation. ChIP-Seq was accomplished by immunoprecipitating endogenous RNA PolII, c-Myc and Sox2

2015-02-18 | E-GEOD-62513 | biostudies-arrayexpress

c-Myc Transcriptionally Amplifies Sox2 Target Genes to Regulate Self-Renewal in Multipotent Otic Progenitor Cells [RNA-Seq]

Project description:An immortalized multipotent otic progenitor (iMOP) cell was generated by transient expression of c-Myc in Sox2-expressing otic progenitor cells. The procedure activated endogenous c-Myc expression in the cells and amplified existing Sox2-dependent transcripts to promote self-renewal. Downregulation of c-Myc expression following growth factor withdrawal resulted in a molecular switch from self-renewal to otic differentiation. Progenitor cells from embryonic inner ear that form otospheres were infected with a c-Myc retrovirus to promote self-renewal

2015-02-18 | E-GEOD-62512 | biostudies-arrayexpress

c-Myc Transcriptionally Amplifies Sox2 Target Genes to Regulate Self-Renewal in Multipotent Otic Progenitor Cells [RNA-Seq]

2015-02-18 | GSE62512 | GEO

c-Myc Transcriptionally Amplifies Sox2 Target Genes to Regulate Self-Renewal in Multipotent Otic Progenitor Cells [ChIP-Seq]

2015-02-18 | GSE62513 | GEO

Identification the Expression of Sox2 in Colorectal Cancer Tissues

Project description:Sox2 has been studied in several types of human solid tumors. The investigators found that Sox2 had higher expression level in colorectal cancer and metastatic tissues than normal tissues. So the investigators assumed that whether Sox2 plays an important role in the progression and migration of colon cancer.

| 2124687 | ecrin-mdr-crc

Elevating Sox2 levels deleteriously affects the growth of glioblastoma and medulloblastoma cells.

Project description:Induction of the transcription factor Sox2 from a doxycycline-inducible promoter in iSox2-DAOY medulloblastoma cells. Affymetrix microarrays were used to characterize the gene expression profile of iSox2-DAOY cells in the absence and presence of doxycycline. Human DAOY medulloblastoma cells were engineered to express epitope tagged Sox2 under the control of a doxycycline inducible promoter, to produce iSox2-DAOY cells. iSox2-DAOY cells were FACS sorted into CD133 low and high populations. The CD133 low population was cultured in the absence and presence of 0.5 Âµg/mL doxycycline for 24 hours. RNA was extracted from cells cultured without and with doxycycline, and was used for microarray analysis.

2012-08-25 | E-GEOD-36947 | biostudies-arrayexpress

Elevating Sox2 levels deleteriously affects the growth of glioblastoma and medulloblastoma cells.

2012-08-25 | GSE36947 | GEO

Transcription profiling of mouse in vitro reprogrammed fibroblasts carrying retroviral transgenes for Oct4, Sox2, Klf4, and c-Myc to investigate developmental potential

Project description:Comparison of in vitro reprogrammed fibroblasts carrying retroviral transgenes for Oct4, Sox2, Klf4, and c-Myc with non-infected fibroblasts and wt ES cells.

2007-06-06 | E-MEXP-1037 | biostudies-arrayexpress

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