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Gene Expression Profiling in A549 Lung Cancer Cell Line Following siRNA Mediated Knock-down of ALDH1A1 and ALDH3A1

ABSTRACT: Aldehyde dehydrogenase isozymes ALDH1A1 and ALDH3A1 are highly expressed in non small cell cell lung cancer. Neither the mechanism nor the biological significance for such over expression have been studied. We used microarrays to analyze changes in A549 lung cancer cell line in which ALDH activity was reduced using lentiviral mediated expression of siRNA against both isozymes (Lenti 1+3) Keywords: Gene Profiling after ALDH Knock Down

ORGANISM(S): Homo sapiens

PROVIDER: GSE8045 | GEO | 2008/10/29

SECONDARY ACCESSION(S): PRJNA100867

REPOSITORIES: GEO

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siRNA profiling of human A549 lung cancer cell line following siRNA mediated knock-down of ALDH1A1 and ALDH3A1

Project description:Aldehyde dehydrogenase isozymes ALDH1A1 and ALDH3A1 are highly expressed in non small cell cell lung cancer. Neither the mechanism nor the biological significance for such over expression have been studied. We used microarrays to analyze changes in A549 lung cancer cell line in which ALDH activity was reduced using lentiviral mediated expression of siRNA against both isozymes (Lenti 1+3) Experiment Overall Design: A549 lung cancer cell lines were transduced with lentiviral vectors containing specific siRNA sequences against ALDH1A1, ALDH3A1, both vectors (Lenti 1+3 cells), and against the green flourescent protein (GFP) gene (GFP cells, used as control).

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Project description:Retinaldehyde dehydrogenases convert retinal into all-trans retinoic acid (ATRA), thereby regulating cell differentiation and cancer stem cell proliferation. Chemical tools and methods are valuable commodities to study aldehyde dehydrogenase (ALDH) activity in human cells. Here, we describe the design, synthesis and application of LEI-945, a first-in-class activity-based probe modeled on retinal that reports on individual ALDHs in cancer cells. Comparative chemical proteomics with LEI-945 explained the ability of various breast cancer cell lines to produce ATRA via retinaldehyde dehydrogenases isozymes, whereas the ALDEFLUORTM assay could not. Competitive chemical proteomics using LEI-945 revealed that the ALDH inhibitor NCT-505 inhibited both ALDH1A1 and ALDH1A3 in MDA-MB-468 breast cancer cells inducing a cell cycle arrest in the G1 phase as well as cell death through necrosis. Our results show that LEI-945 holds promise to guide the discovery of ALDH-based therapeutics

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Project description:The goal of this study was to identify preadipocyte signature genes that are dependent in aldehyde dehydrogenase 1a1 (Aldh1a1) by comparison genomes of the immortalized wild type and Aldh1a1-/- preadipocytes. Gene expression was measured using theAffymetrix GeneChip Mouse Gene ST 2.0 arrays. Murine wild type (n=3, control) and Aldh1a1-/- preadipocytes (n=3) were cultured in standard DMEM medium containing 10% of calf serum. mRNA was isolated by RNeasy (Qiagen, Valencia, CA). RNA integrity was interrogated using the Agilent 2100 Bioanalyzer (Agilent Technologies). A 100ng aliquot of total RNA was linearly amplified. Then, 5.5ug of cDNA was labeled and fragmented using the GeneChip WT PLUS reagent kit (Affymetrix, Santa Clara, CA) following the manufacturer's instructions. Labeled cDNA targets were hybridized to Affymetrix GeneChip Mouse Gene ST 2.0 arrays for 16 h at 45 Â°C rotating at 60rpm. The arrays were washed and stained using the Fluidics Station 450 and scanned using the GeneChip Scanner 3000. Signal intensities were quantified by Affymetrix Expression Console version 1.3.1. Background correction and quantile normalization was performed to adjust technical bias, and probe-set expression levels were calculated by RMA method. After filtering above noise cutoff, there are 9,528 probe-sets that were tested by linear model. A variance smoothing method with fully moderated t-statistic was employed for this study and was adjusted by controlling the mean number of false positives. With a combined cutoff of 2-fold change and p-value of 0.0001 (controlling 1 false positive over all probe-sets), we declared 500 probe-sets as differential gene expression between Aldh1a1-/- and WT preadipocytes.

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Project description:Failure to achieve complete elimination of triple negative breast cancer (TNBC) stem cells after adjuvant therapy is associated with poor outcomes. Aldehyde dehydrogenase 1 (ALDH1) is a marker of breast cancer stem cells (BCSCs), and its enzymatic activity regulates tumor stemness. Identifying upstream targets to control ALDH+ cells may facilitate TNBC tumor suppression. Here, we show that KK-LC-1 determines the stemness of TNBC ALDH+ cells via binding with FAT1 and subsequently promoting its ubiquitination and degradation. This compromised the Hippo pathway and led to nuclear translocation of YAP1 and ALDH1A1 transcription. These findings identified the KK-LC-1-FAT1-Hippo-ALDH1A1 pathway in TNBC ALDH+ cells as a therapeutic target. To reverse the malignancy due to KK-LC-1 expression, we employed a novel computational approach and discovered Z839878730 (Z8) as an small-molecule inhibitor which may disrupt KK-LC-1 and FAT1 binding. We demonstrate that Z8 suppressed TNBC tumor growth via a mechanism that reactivated the Hippo pathway and decreased TNBC ALDH+ cell stemness and viability.

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