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Exploration of genes involved in mature B cells-directed inflammation caused by PTEN mutation

ABSTRACT: Exploration of genes involved in mature B cells-directed inflammation caused by PTEN mutation

PROVIDER: PRJNA744759 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15068940_1.fastq.gz	Fastqsanger.gz
	SRR15068940_2.fastq.gz	Fastqsanger.gz
	SRR15068941.fastq.gz	Fastqsanger.gz
	SRR15068942_1.fastq.gz	Fastqsanger.gz
	SRR15068942_2.fastq.gz	Fastqsanger.gz

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Exploration of genes involved in mature B cells-directed inflammation caused by PTEN mutation

Project description:To expose additional genes and signaling pathways involved in the B cell-mediated inflammation in CD23-cKO mice, we performed single-cell RNA-sequencing (scRNA-seq) transcriptomic analysis. These data suggest that the induction of TLR9-mediated IL-6 production triggered by PTEN deficiency relies on BCR-directed endocytosis.

2024-07-08 | GSE179715 | GEO

Pax5 regulates B cell immunity by promoting PI3K signaling via PTEN downregulation

Project description:The transcription factor Pax5 is known to control B-cell development, but its role in mature B- cells is largely enigmatic. Here, we demonstrate by conditional mutagenesis in peripheral B- lymphocytes that B-1a, marginal zone (MZ) and germinal center B-cells as well as plasma cells are not generated upon loss of Pax5. Follicular (FO) B-cells tolerate the loss of Pax5 but have a shortened half-life. The Pax5-deficient FO B-cells fail to proliferate upon B-cell receptor or Toll- like receptor stimulation due to impaired PI3K-AKT signaling, which is caused by increased expression of PTEN, a negative regulator of the PI3K pathway. Pax5 restrains PTEN protein expression at the posttranscriptional level, likely involving Pten-targeting microRNAs. Additional PTEN loss in Pten,Pax5 double-mutant mice rescues FO B-cell numbers and the development of MZ B-cells. Hence, the posttranscriptional downregulation of PTEN expression is a dominant function of Pax5 that facilitates the differentiation and survival of mature B cells, thereby promoting humoral immunity.

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Transcriptomics of PTEN knockout B16-F10 cells in C57BL/6J mice model treated with PTEN

Project description:extracellular PTEN treatment did not affect the growth of PTEN knockout B16-F10 cells cultured in vitro. , To investigate whether extracellular PTEN act on the tumor microenvironment to exert a tumor-suppressive role in vivo，molecular changes caused by PTEN treatment inside the B16-F10-PTEN tumors were monitored by RNA sequencing.

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miRNA expression in PTEN-deficient premalignant DP thymocytes

Project description:T cell-specific deletion of PTEN induces premalignancy in CD4+ CD8+ (DP) immature T cells in the thymus, which progresses to the development of mature CD4+ T cell lymphomas in the lymph nodes and spleen. As part of a screen to identify factors that inhibit progression to malignancy, we compared miRNA expression in premalignant PTEN-deficient DP thymocytes versus wild-type controls. DP thymocytes were collected by cell sorting from three 9-week-old, premalignant T cell-specific PTEN-deficient mice (tPTEN-/-) and three littermate controls. miRNA expression was assessed relative to a reference pool generated from an equal mixture of all samples.

2014-04-12 | E-GEOD-56759 | biostudies-arrayexpress

Pten

Project description:Drosophila melanogaster Pten, Phosphatase and tensin homolog, is differentially expressed in 8 experiment(s);

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Project description:Drosophila melanogaster Pten, Phosphatase and tensin homolog, is expressed in 4 baseline experiment(s);

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miRNA expression in PTEN-deficient premalignant DP thymocytes

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

Project description:Nuclear localization of PTEN is essential for its tumor suppressive role, and loss of nuclear PTEN is more prominent than cytoplasmic PTEN in many kinds of cancers. However, nuclear PTEN-specific regulatory mechanisms were rarely reported. Based on the finding that nuclear PTEN is more unstable than cytoplasmic PTEN. Thus, 293T cells were transiently transfected with plasmid encoding Flag-tagged PTEN along with empty vector, followed by affinity purification using an anti-Flag antibody, and the bound proteins were analyzed by liquid chromatography with tandem mass spectrometry (LC−MS/MS). Here we identify that F-box only protein 22 (FBXO22) induces ubiquitylation of nuclear but not cytoplasmic PTEN at lysine 221, which is responsible for the degradation of nuclear PTEN.

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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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