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Transcriptomic study with knock-in of PIK3CD in tumoral experimental mouse model

ABSTRACT: Transcriptomic study with knock-in of PIK3CD in tumoral experimental mouse model

PROVIDER: PRJNA760473 | ENA |

REPOSITORIES: ENA

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Transcriptomic study with knock-in of PIK3CD in tumoral experimental mouse model

Project description:The isoform delta of class I Phosphoinositide 3-kinase (PI3Kdelta) is expressed primarily in hematopoietic cells, and its inhibitor, idelalisib, is approved for the treatment of leukemia and lymphoma. PI3Kdelta orients the apicobasal axis and regulates lumen formation through assembly of the extracellular matrix. PI3Kdelta overexpression in hepatocellular carcinoma (HCC) cells (Huh7) leads to profound changes in cell morphogenesis and is associated to the up-regulation of stem cell markers. With tumoral experimental mouse model, investigations on PI3Kdelta implication were performed after knock-in transfection

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Comparative expression data of PD21 Pik3cd+/- and Pik3cd-/- female mice ovaries responsed to exogenous gonadotropins.

Project description:The Pik3cd null females are subfertile and have less growing follicles than their heterozygous littermates in the ovary. These mice poorly respond to the exogenous gonadotropins and ovulate much less oocytes than controls. In addition, the estrodial stimulated GC proliferation in preantral follicles is also impaired in Pik3cd null ovaries. FSH and E2 dramatically activates PI3K/AKT pathway in GCs of wild type mice, but not in the Pik3cd null mice. we used microarray to identify those genes regulated by Pik3cd in response to PMSG (Pregnant Mare Serum Gonadotropin) and E2 treatment in ovary. We set 3 treatment groups of both Pik3cd+/- and Pik3cd-/- female mice, including PD21 untreatment, PD21 after PMSG administration for 44 hours, PD21 after E2 administration for 72 hours, each group contained three biological repeats. The genes up/down-regulated significantly (not less than 2 fold change) in Pik3cd+/- mice after PMSG and E2 treatment were listed out as PMSG or E2 target genes, in which, those had not the same change trends in Pik3cd-/- were considered as Pik3cd-dependent genes.

2012-10-23 | E-GEOD-41746 | biostudies-arrayexpress

Comparative expression data of PD21 Pik3cd+/- and Pik3cd-/- female mice ovaries responsed to exogenous gonadotropins.

2012-10-23 | GSE41746 | GEO

Autosomal recessive PIK3CD deficiency

Project description:Autosomal recessive PIK3CD deficiency

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Autosomal recessive PIK3CD deficiency

Project description:We studied a case with suspected PIK3CD deficiency with a homozygous mutation in the patient in PIK3CD (c.1340-1 G>A). All other family members were tested and defined as carriers of the same mutation and are clinically healthy. The literature states that there is an AD but also an AR form of the disease (Immunodeficiency 14 A and B, respectively) linked to the gene. The clinical phenotype of the patient fits very well the description as LOF she suffers from severe, recurrent infections since infancy and has low overall IgG levels.

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The long non-coding RNA PIK3CD-AS2 promotes lung adenocarcinoma progression via YBX1-mediated suppression of p53 pathway

Project description:The underlying mechanisms of long non-coding RNAs (lncRNA) participating in the progression of lung cancers are largely unknown. We found a novel lncRNA, PIK3CD antisense RNA 2 (PIK3CD-AS2), that contributes to lung adenocarcinoma (LUAD) progression. The expression characteristics of PIK3CD-AS2 in LUAD were analyzed using microarray expression profile, The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) datasets, and validated in 92 paired LUAD tissues by chromogenic in situ hybridization. Our data confirmed that PIK3CD-AS2 expression is a crucial regulator of LUAD progression and associated with shorter patient survival. In vitro studies showed that PIK3CD-AS2 increased cell growth and slowed apoptosis in p53wt cells but not in p53null cells. Mechanically, it is demonstrated that PIK3CD-AS2 bound to and maintained the stability of Y-box binding protein 1 (YBX1), a potent destabilizer of p53, by impeding its ubiquitination and degradation. Downexpression of YBX1 reversed PIK3CD-AS2-mediated inhibition of p53 signaling. Additionally, the therapeutic effect evaluation of a Locked Nuclear Acid (LNA) specifically targeting PIK3CD-AS2 showed an anti-tumor activity in mice with A549 cells xenograft and p53 wild-type LUAD patient-derived tumor xenograft (PDTX) model. Clinically, the high expression of PIK3CD-AS2 showed a poor disease-free survival in p53 wild-type patients in TCGA database. Our findings suggest that PIK3CD-AS2 regulates LUAD progression and elucidate a new PIK3CD-AS2/YBX1/p53 signaling axis, providing a potential lncRNA-directed therapeutic strategy especially in p53 wild-type LUAD patients.

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