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Gene expression profile for NGAL overexpression in esophageal squamous carcinoma cell

ABSTRACT: Neutrophil gelatinase associated lipocalin (NGAL), also known as oncogene 24p3, uterocalin, siderocalin or lipocalin 2 (Lcn2), is a member of the lipocalin family. Elevated NGAL involves various functions in malignant cells, even sometimes the conclusions were controversial. NGAL inhibits apoptosis in thyroid cancer and decrease invasion and angiogenesis in pancreatic cancer, but it increase proliferation and metastasis in breast and colon cancer. Nonetheless, the molecular functions and mechanisms of NGAL in ESCC are unknown. To address these issues and to identify genes and biological pathways associated with NGAL functions and mechanism, NGAL was overexpressed by pcDNA3.0 plasmid in ESCC cell line EC109 with an empty plasmid as a control, these two cells were applied for mRNA expression profile analyses to find the differentially expressed genes. Plasmids of pcDNA3.0-NGAL and pcDNA3.0 were transfected into ESCC cell line EC109, respectively. Stable transfected cell clones were selected by G418. The overexpression of NGAL protein was confirmed by western blot. Total RNAs from NGAL overexpressed cells and control cells were extracted for Agilent whole genome oligo microarray. A dye flip was performed for duplicate.

ORGANISM(S): Homo sapiens

SUBMITTER: Enmin Li

PROVIDER: E-GEOD-57630 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene expression profile for NGAL overexpression in esophageal squamous carcinoma cell

Project description:Neutrophil gelatinase associated lipocalin (NGAL), also known as oncogene 24p3, uterocalin, siderocalin or lipocalin 2 (Lcn2), is a member of the lipocalin family. Elevated NGAL involves various functions in malignant cells, even sometimes the conclusions were controversial. NGAL inhibits apoptosis in thyroid cancer and decrease invasion and angiogenesis in pancreatic cancer, but it increase proliferation and metastasis in breast and colon cancer. Nonetheless, the molecular functions and mechanisms of NGAL in ESCC are unknown. To address these issues and to identify genes and biological pathways associated with NGAL functions and mechanism, NGAL was overexpressed by pcDNA3.0 plasmid in ESCC cell line EC109 with an empty plasmid as a control, these two cells were applied for mRNA expression profile analyses to find the differentially expressed genes.

2014-05-14 | GSE57630 | GEO

CD4 T cell response in AKI

Project description:CD4+ T cells mediate the pathogenesis of ischemic and nephrotoxic acute kidney injury (AKI), as well as acute injury to other organs. However, the underlying mechanisms of CD4+ T cell-mediated pathogenesis are largely unknown. We therefore conducted unbiased RNA-sequencing to discover novel mechanistic pathways of kidney CD4+ T cells post-ischemia compared to normal mouse kidney. Unexpectedly, lipocalin-2 (Lcn2) gene, which encodes neutrophil gelatinase-associated lipocalin (NGAL) had the highest (~60)-fold increase. The NGAL increase in CD4+ T cells during AKI was confirmed at the mRNA level with real-time PCR and at the protein level with ELISA. NGAL is a potential biomarker for the early detection of AKI and has multiple potential biological functions during organ injury. However, the role of NGAL produced by CD4+ T cells has not been investigated. We found that ischemic AKI in NGAL knockout (KO) mice had worse renal outcomes compared to wild type (WT) mice. Adoptive transfer of NGAL-deficient CD4+ T cells from NGAL KO mice into CD4 KO or WT mice led to worse renal function than transfer of WT CD4+ T cells. In vitro simulated ischemia reperfusion showed that NGAL-deficient CD4+ T cells express higher levels of IFN-γ mRNA compared to WT CD4+ T cells. In vitro differentiation of naive CD4+ T cells to Th17, Th1 and Th2 cells led to significant increase in Lcn2 expression. Human kidney CD4+ T cell NGAL also increased significantly post-ischemia. These results demonstrate an important role for CD4+ T cell NGAL as a mechanism by which CD4+ T cells mediate AKI and extend the importance of NGAL in AKI beyond diagnostics.

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TgFVB vs FVB 6 and 8 week kidneys

Project description:Human Immunodeficiency Virus (HIV) associated nephropathy (HIVAN) is characterized clinically by both nephrosis and by rapidly progressive kidney dysfunction. HIVAN is characterized histologically by both collapsing focal segmental glomerulosclerosis and prominent tubular damage. Neutrophil Gelatinase Associated Lipocalin (NGAL) is known to be rapidly expressed in distal segments of the nephron at the onset of different types of acute kidney injury, but few studies have examined NGAL in chronic kidney disease models. We found that urinary NGAL (uNGAL) was highly expressed by patients with biopsy proven HIVAN, whereas HIV+ patients without HIVAN demonstrated lower levels. uNGAL was also highly expressed in the TgFVB mouse model of HIVAN, which demonstrated NGAL gene expression in dilated, microcystic segments of the nephron. These data show that NGAL is markedly upregulated in the setting of HIVAN, and suggest that uNGAL levels may provide a non-invasive screening test to detect HIVAN related tubular disease. Microarray data revealed that NGAL was one of the most highly upregulated gene the TgFVB mouse.

2009-12-25 | E-GEOD-14221 | biostudies-arrayexpress

TgFVB vs FVB 6 and 8 week kidneys

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Diagnostic and Prognostic Significance of Serum Neutrophil Gelatinase-Associated Lipocalin in Patients with Colorectal Cancer

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Increased Susceptibility to AKI in a Mouse Model of Presymptomatic Cardiomyopathy

Project description:The early events that signal renal dysfunction in presymptomatic heart failure are unclear. To evaluate this, we performed RNA-seq on kidneys from transgenic mice with cardiac-specific overexpression of mutant alpha-B-crystallin, which develop slowly progressive cardiomyopathy. Presymptomatic transgenic mice display an increase in serum creatinine and in urinary neutrophil gelatinase-associated lipocalin (NGAL), but lack chronic interstitial fibrosis. Presymptomatic transgenic mouse kidneys exhibited a worsened response to ischemia-reperfusion injury based on serum creatinine, urine NGAL, tubule dilation and cast score, and apoptosis. Our findings demonstrate functional renal impairment, urinary biomarker elevations, and gene expression changes that occur in early presymptomatic heart failure, which dramatically increase the susceptibility to subsequent acute kidney injury.

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siRNA profiling of human ezrin-knockdown ec109 cells(PSE1) and control(PS)

Project description:Ezrin belongs to the ezrinÂ¨CradixinÂ¨Cmoesin (ERM) family proteins, which cross-link actin cytoskeleton and plasma membrane, and is actively involved in regulating the growth and metastatic capacity of cancer cells. Esophageal squamous cell carcinoma (ESCC) is one of the most fatal malignancies in the world and the expression of ezrin in ESCC has been described only recently, but its roles and mechanism still remained unclear. we have used the pSUPER RNAi system to stably suppress the expression of the ezrin gene in EC109, an esophageal squamous carcinoma cell line, and then cDNA microarray was performed to explore some changed genes with ezrin silence. Experiment Overall Design: he mammalian expression vector, pSUPER.neo.circular (OligoEngine), was used for expression of siRNA in EC109 cells. Briefly, two primer pairs were synthesized, one pair encoding nucleotides 274Â¨C292 (TCCACTATGTGGATAATAA) followed by a 9 base Â¡Â®Â¡Â®loopÂ¡Â¯Â¡Â¯ (TTCAAGAGA) and the inverted repeat (PSE1), and the second encoding nucleotides 265Â¨C283 (ACTTTGGCCTCCACTATGT) again followed by the loop and inverted repeat (PSE2). And pSUPER.neo vector of nonspecific siRNA was taken as negative control (PSC). The primer pairs were annealed and inserted into the BglII and HindIII sites of pSUPER.neo and transformed into JM109 competent cells (Promega). Positive clones were verified and transfected into EC109 cells using FuGENE 6 transfection reagent (Roche) according to the manufacturerÂ¡Â¯s instructions. G418 (400 Â¦Ãg/ml, Calbiochem) was added into the culture medium after 24 h. Stable G418-resistant clones were obtained in 7Â¨C9 days. The expanded cells were then used for subsequent studies.

2008-06-14 | E-GEOD-6233 | biostudies-arrayexpress

MicroRNA profiling by array of mouse prostate cancer cell lines treated with dihydrotestosterone and prostate xenografts in intact or castrated mice

Project description:Effect of dihydrotestosterone and castration on microRNA expression

2011-02-25 | E-MEXP-2602 | biostudies-arrayexpress

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2008-06-13 | E-GEOD-5478 | biostudies-arrayexpress

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