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SOX2 is required independently in both stem and differentiated cells for pituitary tumor genesis in p27 null mice III

ABSTRACT: SOX2 is required independently in both stem and differentiated cells for pituitary tumor genesis in p27 null mice III

PROVIDER: PRJNA638094 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11952691.fastq.gz	Fastqsanger.gz
	SRR11952692.fastq.gz	Fastqsanger.gz
	SRR11952693.fastq.gz	Fastqsanger.gz

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Similar Datasets

SOX2 is required independently in both stem and differentiated cells for pituitary tumor genesis in p27 null mice II

Project description:Characterization of the effects of Sox2 heterozygosity on tumorigenesis in p27-/- pituitary tumors.

2021-02-24 | GSE152008 | GEO

SOX2 is required independently in both stem and differentiated cells for pituitary tumor genesis in p27 null mice

Project description:SOX2 is required independently in both stem and differentiated cells for pituitary tumor genesis in p27 null mice

| PRJNA638090 | ENA

SOX2 is required independently in both stem and differentiated cells for pituitary tumor genesis in p27 null mice I

Project description:SOX2 is required independently in both stem and differentiated cells for pituitary tumor genesis in p27 null mice I

| PRJNA638092 | ENA

SOX2 is required independently in both stem and differentiated cells for pituitary tumor genesis in p27 null mice II

Project description:SOX2 is required independently in both stem and differentiated cells for pituitary tumor genesis in p27 null mice II

| PRJNA638093 | ENA

SOX2 is required independently in both stem and differentiated cells for pituitary tumor genesis in p27 null mice I

Project description:Characterization of the initiation and development of pituitary intermediate lobe tumors in p27-/- mice.

2021-02-24 | GSE152007 | GEO

SOX2 is required independently in both stem and differentiated cells for pituitary tumor genesis in p27 null mice III

Project description:Exploration of the molecular mechanisms underlying melanotroph tumourigenesis and the role of SOX2 in both SCs and melanotrophs

2021-02-24 | GSE152009 | GEO

SOX2 is required independently in both stem and differentiated cells for pituitary tumor genesis in p27 null mice

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

2021-02-24 | GSE152010 | GEO

SOX2 is required independently in both stem and differentiated cells for pituitary tumorigenesis in <i>p27</i>-null mice.

Project description:P27, a cell cycle inhibitor, is also able to drive repression of Sox2 This interaction plays a crucial role during development of p27-/- pituitary tumors because loss of one copy of Sox2 impairs tumorigenesis [H. Li et al., Cell Stem Cell 11, 845-852 (2012)]. However, SOX2 is expressed in both endocrine and stem cells (SCs), and its contribution to tumorigenesis in either cell type is unknown. We have thus explored the cellular origin and mechanisms underlying endocrine tumorigenesis in p27-/- pituitaries. We found that pituitary hyperplasia is associated with reduced cellular differentiation, in parallel with increased levels of SOX2 in stem and endocrine cells. Using conditional loss-of-function and lineage tracing approaches, we show that SOX2 is required cell autonomously in p27-/- endocrine cells for these to give rise to tumors, and in SCs for promotion of tumorigenesis. This is supported by studies deleting the Sox2 regulatory region 2 (Srr2), the target of P27 repressive action. Single cell transcriptomic analysis further reveals that activation of a SOX2-dependent MAPK pathway in SCs is important for tumorigenesis. Altogether, our data highlight different aspects of the role of SOX2 following loss of p27, according to cellular context, and uncover an unexpected SOX2-dependent tumor-promoting role for SCs. Our results imply that targeting SCs, in addition to tumor cells, may represent an efficient antitumoral strategy in certain contexts.

| S-EPMC7896314 | biostudies-literature

Gene misexpression in a Smoc2+ve/ Sox2-low population in juvenile Prop1-mutant pituitary gland

Project description:Mutations in the pituitary specific transcription factor Prophet of Pit-1 (PROP1) are the most common genetic etiology of combined pituitary hormone deficiency (CPHD). CPHD is associated with short stature, attributable to growth hormone deficiency and/or thyroid stimulating hormone deficiency, as well as hypothyroidism and infertility. Pathogenic lesions impair pituitary development and differentiation of endocrine cells. We performed single-cell RNA sequencing of pituitary cells from a wild-type and a Prop1-mutant P4 female to elucidate population-specific differential gene expression. We observed a Smoc2+ve population that expressed low Sox2, which trajectory analyses suggest are a transitional cell state as stem cells differentiate into endocrine cells. We also detected ectopic expression of Sox21 in these cells in the Prop1df/df mutant. Prop1-mutant mice are known to overexpress Pou3f4, which we now show to be also enriched in this Smoc2+ve population. We sought to elucidate the role of Pou3f4 during pituitary development and to determine the contributions of Pou3f4 upregulation to pituitary disease by utilizing double-mutant mice lacking both Prop1 and Pou3f4. However, our data showed that Pou3f4 is not required for normal pituitary development and function. Double mutants further demonstrated that the upregulation of Pou3f4 was not causative for the overexpression of Sox21. These data indicate loss of Pou3f4 is not a potential cause of CPHD, and further studies may investigate the functional consequence of upregulation of Pou3f4 and Sox21, if any, in the novel Smoc2+ve cell population.

2024-08-03 | GSE273683 | 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

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