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HO-1 modulates the expression of genes involved in inflammation, angiogenesis, proliferation, apoptosis and cell adhesion in human lung cancer cells.

ABSTRACT: The enzymatic activity of HO-1 results in decreased oxidative stress, attenuated inflammatory response, and very often in a lower rate of apoptosis. This is due to removal of heme, a potent prooxidant and proinflammatory agent, but mainly because of generation of biologically active products such as CO and bilirubin. In order to find the correlation between the HO-1 level and the expression of different genes of interest we have utilized human lung cancer cell line NCI-H292 stably overexpressing HO-1. Additionally we have checked if HO-1 can modulate genes expression in NCI-H292 cells treated with TNF. The effect of HO-1 overexpression on transcriptome was assessed by microarray analysis. We have observed that the increase in HO-1 level may affect the expression of different genes involved in cytokine synthesis, angiogenesis, apoptosis, proliferation and cell adhesion. Additionally, HO-1 may interact with the TNF treatment and influence the expression of some genes like IL-1, IL-6, IL-8, FAS and NF-kB.

ORGANISM(S): Homo sapiens

PROVIDER: GSE22030 | GEO | 2011/10/19

SECONDARY ACCESSION(S): PRJNA127459

REPOSITORIES: GEO

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Project description:Heme Oxygenase-1 (HO-1) is expressed in many cancers and influences the growth, survivall and metastasis of tumors, however, the molecular mechanisms remains largely unknown. To identify a common mechanism of action of HO-1 in cancer, we studied the global effect of HO-1 on the transcriptome of multiple tumors. Genome-wide expression profiling of HO-1 expressing versus HO-1 silenced cancer cells and a further data mining analysis of the preexisting expression database of 190 human tumors of 14 cancer types led us to identify 14 genes, the expression of which correlated firmly and universally with that of HO-1 (P < 0.001). These genes included regulators of cell plasticity and extracellular matrix remodeling (MMP2, ADAM8, TGFβ1, BGN, COL21A1, PXDN), signaling (CRIP2, MICB), amino acid transport and glycosylation (SLC7A1 and ST3GAL2), estrogen and phospholipid biosynthesis (AGPAT2 and HSD17B1), protein stabilization (IFI30) and phosphorylation (ALPPL2). PXDN, one of the genes being co-expressed with HO-1, was selected for further analysis. Immunofluorescence and western blotting confirmed positive correlation of PXDN with HO-1 levels in BeWo cancer cells as well as co-localization in invasive extravillous trophoblast cells of first trimester placenta. Loss of HO-1 in BeWo cells correlated with reduced cell adhesion to Collagen type I, Fibronectin and Laminin. The adhesion-promoting effects of HO-1 were dependent on PXDN expression, as loss of PXDN in HO-1 expressing BeWo cells led to reduced cell attachment to Laminin and Fibronectin coated wells. We used gene expression profiling to determine the genome-wide effect of HO-1 on the transcriptome of BeWo trophoblast cells. We specifically selected BeWo cells for our studies because these cells express HO-1 naturally. We knocked down endogenous HO-1 in BeWo cells using retroviral transduction with a micro-RNA adapted retroviral vector targeting human HO-1 sequence. RNA isolated from control (LMP) or miHO1 infected (miHO-1) cells was labeled and hybridized to human genome-wide gene level 1.0 ST arrays

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HO-1 modulates the expression of genes involved in inflammation, angiogenesis, proliferation, apoptosis and cell adhesion in human lung cancer cells.

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