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Identification of PARD3 signature on PARD3 deficient H157 cell line, reconstituting the expression of PARD3 gene, with a wt and a mutant form.

ABSTRACT: To development our gene expression approach, we have employed whole genome microarray expression profiling as a discovery platform to identify genes potentialy regulated by the polarity protein PAR3. Human SCC cell line, NCI-H157 (H157), has a big deletion at PARD3 locus and showed no PAR3 protein expression. This cell line was used as a model in which we restored the expression of PAR3 (wt or mutant form). Afterwards, this model was used to identify PARD3 signature on Human SCC.

ORGANISM(S): Homo sapiens

PROVIDER: GSE51506 | GEO | 2015/05/19

SECONDARY ACCESSION(S): PRJNA223392

REPOSITORIES: GEO

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Identification of PARD3 signature on PARD3 deficient H157 cell line, reconstituting the expression of PARD3 gene, with a wt and a mutant form.

Project description:To development our gene expression approach, we have employed whole genome microarray expression profiling as a discovery platform to identify genes potentialy regulated by the polarity protein PAR3. Human SCC cell line, NCI-H157 (H157), has a big deletion at PARD3 locus and showed no PAR3 protein expression. This cell line was used as a model in which we restored the expression of PAR3 (wt or mutant form). Afterwards, this model was used to identify PARD3 signature on Human SCC. There are triplicates of each sample. We compare the effects in gene expression between the different situations: no PARD3 expression in the cell, expression of the mutant form of PARD3 gene and expression of the PARD3 wt form in the cells.

2015-05-19 | E-GEOD-51506 | biostudies-arrayexpress

BET inhibition rescues ciliogenesis and ameliorates pancreatitis-driven phenotypic changes in mice with Par3 loss

Project description:The apical-basal polarity of pancreatic acinar cells is essential for maintaining tissue architecture. However, the mechanisms by which polarity proteins regulate acinar pancreas tissue homeostasis are poorly understood. Here, we evaluate the role of Par3 in acinar pancreas injury and homeostasis. While Par3 loss in the mouse pancreas disrupts tight junctions, Par3 loss is dispensable for pancreatogenesis. However, with aging, Par3 loss results in low-grade inflammation, acinar degeneration, and pancreatic lipomatosis. Par3 loss also exacerbates pancreatitis-induced acinar cell loss, resulting in pronounced pancreatic lipomatosis and failure to regenerate. Moreover, Par3 loss in mice harboring mutant Kras causes extensive pancreatic intraepithelial neoplastic (PanIN) lesions and large pancreatic cysts. We also show that Par3 loss restricts injury-induced primary ciliogenesis. Significantly, targeting BET proteins enhances primary ciliogenesis during pancreatitis-induced injury and, in mice with Par3 loss, limits pancreatitis-induced acinar loss and facilitates acinar cell regeneration. Combined, this study demonstrates how Par3 restrains pancreatitis- and Kras-induced changes in the pancreas and identifies a potential role for BET inhibitors to attenuate pancreas injury and facilitate pancreas tissue regeneration.

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A genome-wide screen for microdeletions reveals disruption of polarity complex genes in diverse human cancers

Project description:In a genome-wide screen of human cancer cell lines, we identified homozygous intragenic microdeletions involving genes encoding components of the apical-basal cell polarity complexes. Among these, PARD3 is disrupted in cell lines and primary tumors from squamous carcinomas and glioblastomas. Reconstituting PARD3 expression in both cell types restores tight junctions and retards contact-dependent proliferation. Searching specifically for small intragenic microdeletions using high-resolution genomic arrays may be complementary to other genomic deletion screens and resequencing efforts in identifying new tumor suppressor genes.

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Targeting of Tumor Cells by the Adenovirus E4orf4 protein via Par3 Polarity Protein-Regulated Nuclear Envelope Rupture

Project description:The protein product of the Early region 4 open reading frame 4 (E4orf4) of human adenovirus 2 is reported to exhibit a tumor-selective cell killing activity. Here, we show that E4orf4’s tumoricidal activity correlated with changes in perinuclear actomyosin contractility that are controlled by an interaction with the Par3 polarity protein. Surprisingly, E4orf4 enhanced apical-basal polarity in non-transformed mammary epithelial cells. In contrast, in tumorigenic cells, it induced a high incidence of actin-dependent nuclear bleb rupture. This process, which was regulated by the linker of nucleoskeleton and cytoskeleton (LINC) complex, promoted nuclear efflux of E4orf4 and the breakdown of the nuclear compartment. Significantly, Par3 also regulated the incidence of transient nuclear envelope rupture due to the reduced nuclear rigidity in cells depleted of lamins, in absence of E4orf4. Thus, using E4orf4 as a probing tool, we uncovered a so far un-appreciated role for Par3 in controlling the actin-dependent forces acting on the nuclear envelope to remodel nuclear shape, which might be a defining feature of tumor cells that is harnessed by E4orf4.

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A genome-wide screen for microdeletions reveals disruption of polarity complex genes in diverse human cancers

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Cell polarity proteins promote macropinocytosis in response to metabolic stress

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