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Germline PTEN promoter variants affect the expression profile in breast tumors

ABSTRACT: Comparison of the tumors PTEN promoter variant carrier and non carrier gene expression profiles. Expression profiles of 10 breast cancer patients with PTEN promoter variant and 10 controls matches for histology, ER, PR, T, N, M, Grade, HER2, Ki67, and p53.

ORGANISM(S): Homo sapiens

SUBMITTER: Dario Greco

PROVIDER: E-GEOD-22652 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Germline PTEN promoter variants affect the expression profile in breast tumors

Project description:Comparison of the tumors PTEN promoter variant carrier and non carrier gene expression profiles.

2011-07-01 | GSE22652 | GEO

Germline PTEN promoter variants affect the expression profile in breast tumors

Project description:Comparison of the tumors PTEN promoter variant carrier and non carrier gene expression profiles. Expression profiles of 10 breast cancer patients with PTEN promoter variant and 10 controls matches for histology, ER, PR, T, N, M, Grade, HER2, Ki67, and p53.

| S-ECPF-GEOD-22652 | biostudies-other

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Project description:Transposase-accessible chromatin using sequencing (ATAC-seq) assay was performed to compare chromatin open regions (OCRs) between PTEN-KD and PTEN/BRG1-KD 22RV-1 cells. Ablation of BRG1 in PTEN-depleted cells preferentially led to the reductions of OCR at enhancers, but not promoter regions.

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RNA sequencing of PTEN,Rb1 double knockout (DKO) mouse prostate organoids treated with vehicle or the small molecule mitochondrial pyruvate carrier (MPC) inhibitor UK5099

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PTEN-L induce PTEN-null tumor cells dormancy but lung outgrowth.

Project description:PTEN is one of the most frequently mutated tumor suppressor genes, its loss has been reported in multiple tumor types and is associated with a poor outcome. PTEN-L, as a secreted isoform of PTEN, with the ability to enter cells and inhibit tumor cell growth via inhibiting AKT mediated cell proliferation. However, the distinct effect of PTEN-L on PTEN-expression or PTEN-loss tumor cells is not known yet. Here, we identified PTEN-L treatment facilitate E0771-PTEN-null tumor cells, but not PTEN-wide-type tumor cells lung outgrowth. RNA-seq and Western blot analysis suggest PTEN-L stimulation induced PTEN-null tumor cells dormancy, namely, upregulation of dormancy markers p16 and p27, cell cycle arrest, reduced cell proliferation and chemotherapy drugs resistance. Further study suggested PTEN-L mediated p38 signaling activation play the major role for PTEN-null tumor cell dormancy. The p38 inhibitor, SB202190 significantly reversed the PTEN-L induced PTEN-null tumor cells dormancy and outgrowth in lungs. Further investigation indicated the dormant PTEN-null tumor cells could escape from immunosurveillance and thus outgrowth in lungs, as PTEN-L did not promote PTEN-null tumor cells outgrowth in lung of SCID mice. Therefore, we propose that PTEN-L protects PTEN-null tumor cells from immune attack during lung metastasis via activating dormancy related pathways. This study identified PTEN-L as an activator of PTEN-loss tumor cells dormancy, which enables the efficient seeding and outgrowth of tumor cells in metastatic niches. Overall, we highlight PTEN expression status decides the outcome of PTEN-L mediated anti-tumor therapy.

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Immunoprecipitation of PTEN coupled Nano-LC−ESI-MS/MS

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PTEN modulates gene transcription by redistributing genome-wide RNA polymerase II occupancy [RNA-seq]

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PTEN modulates gene transcription by redistributing genome-wide RNA polymerase II occupancy [ChIP-seq]

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PTEN interacts with the transcription machinery on chromatin and regulates RNA polymerase II-mediated transcription [Affymetrix]

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