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

ABSTRACT: 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

ORGANISM(S): Mus musculus

PROVIDER: GSE183392 | GEO | 2021/09/05

REPOSITORIES: GEO

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Project description:Purpose: The most clearly established genetic hallmark in oligodendroglial tumors (OTs) is the combined loss of 1p/19q, a molecular alteration characteristic of tumors responding to therapy. Markers of tumoral progression have not yet been studied. Experimental Design: Novel markers of tumoral progression in OTs were sought through gene expression profiling analysis. Results: Unsupervised hierarchical cluster analysis classified OTs into two main groups associated with tumoral grade, independent of histological subtype and 1p/19q status. Differential gene expression analysis between low- and high-grade OTs revealed that only cell cycle-related genes were significantly upregulated in high-grade OTs. Among the deregulated genes, NDRG2 downregulation was detected in high-grade OTs with combined loss of 1p/19q. Expression analysis revealed low transcript levels of NDRG2 relative to non-tumoral brain tissue in 45% (9/20) of high-grade OTs. Furthermore, the low transcript levels of NDRG2 were significantly associated with a worse clinical outcome in patients. Transcript levels of NDRG2 were associated with promoter hypermethylation, which was detected in 38.4% (10/26) of high-grade OTs. The treatment of glioma cell lines T98 and LN18 with demethylating agents increased the mRNA expression levels of NDRG2 relative to the control cell line. Additionally, cell proliferation was significantly reduced and cell cycle was arrested in G1 phase after treatment with demethylating agents. Conclusions: Taken together, our results suggest that NDRG2 is a candidate tumor suppressor gene in OTs whose inactivation could be involved in tumoral progression and worse patient survival. The microarray study involved 28 glioma samples including oligodendrogliomas and oligoastrocytomas WHO grade II and III. Six non-tumoral brain tissues were used as controls, two of which were purchased from Stratagene (La Jolla, CA) and Clontech (Mountain View, CA). RNAs from several cell lines (Universal Human RNA, Stratagene, La Jolla, CA) was used as a standard reference in all hybridizations

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

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