Gene expression differences between the microsatellite instability (MIN) and chromosomal instability (CIN) phenotypes in colorectal cancer revealed by high-density cDNA array hybridization

Dunican, Donncha S.; McWilliam, Peter; Tighe, Orna; Parle‐McDermott, Anne; Croke, David T.

doi:10.1038/sj.onc.1205431

Cited by 116 publications

(83 citation statements)

References 15 publications

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“…It is of note that arrayed MMR genes (MSH2, MSH3, MLH1, MLH3, PMS1 and PMS2) were not among these genes. As reported for cell lines (Dunican et al, 2002), several of deregulated genes are involved in cell cycle control, mitosis, transcription and/or chromatin structure (RAN, PTPN21, TP53, MORF4L1, ZFP36L2, PSEN1, IGF2, ASNS, RPS4X, CCNF, ZNF354A). The top downregulated gene in MSI þ tumours was EIF3S2, which encodes the eukaryotic translation initiation factor 3, subunit 2b, also known as TRIP1.…”

Section: Expression Profiles and Msi Phenotypesupporting

confidence: 53%

Gene expression profiling of colon cancer by DNA microarrays and correlation with histoclinical parameters

et al. 2004

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Different diagnostic and prognostic groups of colorectal carcinoma (CRC) have been defined. However, accurate diagnosis and prediction of survival are sometimes difficult. Gene expression profiling might improve these classifications and bring new insights into underlying molecular mechanisms. We profiled 50 cancerous and noncancerous colon tissues using DNA microarrrays consisting of B8000 spotted human cDNA. Global hierarchical clustering was to some extent able to distinguish clinically relevant subgroups, normal versus cancer tissues and metastatic versus nonmetastatic tumours. Supervised analyses improved these segregations by identifying sets of genes that discriminated between normal and tumour tissues, tumours associated or not with lymph node invasion or genetic instability, and tumours from the right or left colon. A similar approach identified a gene set that divided patients with significantly different 5-year survival (100% in one group and 40% in the other group; P ¼ 0.005). Discriminator genes were associated with various cellular processes. An immunohistochemical study on 382 tumour and normal samples deposited onto a tissue microarray subsequently validated the upregulation of NM23 in CRC and a downregulation in poor prognosis tumours. These results suggest that microarrays may provide means to improve the classification of CRC, provide new potential targets against carcinogenesis and new diagnostic and/or prognostic markers and therapeutic targets.

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Section: Expression Profiles and Msi Phenotypesupporting

confidence: 53%

Gene expression profiling of colon cancer by DNA microarrays and correlation with histoclinical parameters

et al. 2004

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“…11 In cancer, BTF3 is found to be overexpressed in glioblastoma multiforme 12 and sporadic colorectal cancer. 13 We have previously identified BTF3 as a differentially expressed gene in PDAC and chronic pancreatitis (CP). 14,15 In the present study we: (1) analyzed the expression of BTF3 mRNA and protein in the normal and diseased pancreas (CP and PDAC) and pancreatic cancer cell lines, and the localization of BTF3 in these tissues; (2) analyzed the functional consequences of BTF3 silencing in pancreatic cancer cell lines in terms of resistance to chemo/radiotherapy-induced apoptosis, and (3) used a DNA micro-array analysis to identify regulation of genes after BTF3 silencing, in order to specify the role of BTF3 in the transcriptional regulation of tumor-associated genes.…”

Section: Introductionmentioning

confidence: 99%

Basic transcription factor 3 (BTF3) regulates transcription of tumor-associated genes in pancreatic cancer cells

Kusumawidjaja

Kayed

Giese

et al. 2007

Cancer Biology & Therapy

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Basic transcription factor 3 (BTF3) acts as a transcription factor and modulator of apoptosis, and is differentially expressed in colorectal cancer and glioblastomas. In the present study, the expression of BTF3, as well as its role in apoptosis and gene transcription, was analyzed in pancreatic ductal adenocarcinoma (PDAC). QRT-PCR, immunohistochemistry, immunoblotting, and immunofluorescence analyses were carried out to investigate BTF3 mRNA/protein expression and localization. BTF3 silencing in pancreatic cancer cells was performed using specific siRNA molecules. Functional analyses were carried out using cell growth assays, apoptosis assays, and DNA array analysis. BTF3 and BTF3a exhibited 1.3-fold and 4.6-fold increased median mRNA levels in PDAC tissues, compared to normal pancreatic tissues. BTF3 localized mainly in the cytoplasm and nuclei of tubular complexes and pancreatic cancer cells. Pancreatic cancer cell lines expressed the mRNA and protein of BTF3a (27 kDa) and BTF3b (22 kDa) isoforms. BTF3 silencing using specific siRNA molecules did not influence apoptosis induced by chemotherapy or radiotherapy. In contrast, BTF3 silencing resulted in down-regulation of several cancer-associated genes, including EPHB2, ABL2, HPSE2 and ATM, and up-regulation of KRAG, RRAS2, NFk-B, MRVI1, MADCAM1 and others. In conclusion, BTF3 is overexpressed in PDAC, where it acts as a transcriptional regulator rather than a direct modulator of apoptosis.

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“…PTPD1 regulates signaling induced by Tec family members of membrane receptors (19) and associates with KIF1C, a tyrosine-phosphorylated kinesin-like protein that controls retrograde transport of vesicles from the Golgi apparatus to the endoplasmic reticulum (20). Expression of PTPD1 is significantly elevated in several human cancers (21).…”

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confidence: 99%

Protein-tyrosine Phosphatase PTPD1 Regulates Focal Adhesion Kinase Autophosphorylation and Cell Migration

Carlucci

Gedressi

Lignitto

et al. 2008

Journal of Biological Chemistry

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PTPD1 is a cytosolic nonreceptor tyrosine phosphatase and a positive regulator of the Src-epidermal growth factor transduction pathway. We show that PTPD1 localizes along actin filaments and at adhesion plaques. PTPD1 forms a stable complex via distinct molecular modules with actin, Src tyrosine kinase, and focal adhesion kinase (FAK), a scaffold protein kinase enriched at adhesion plaques. Overexpression of PTPD1 promoted cell scattering and migration, short hairpin RNA-mediated silencing of endogenous PTPD1, or expression of PTPD1 mutants lacking either catalytic activity (PTPD1 C1108S ) or the FERM domain (PTPD1 ⌬1-325 ) significantly reduced cell motility. PTPD1 and Src catalytic activities were both required for epidermal growth factor-induced FAK autophosphorylation at its active site and for downstream propagation of ERK1/2 signaling. Our findings demonstrate that PTPD1 is a component of a multivalent scaffold complex nucleated by FAK at specific intracellular sites. By modulating Src-FAK signaling at adhesion sites, PTPD1 promotes the cytoskeleton events that induce cell adhesion and migration.

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Gene expression differences between the microsatellite instability (MIN) and chromosomal instability (CIN) phenotypes in colorectal cancer revealed by high-density cDNA array hybridization

Cited by 116 publications

References 15 publications

Gene expression profiling of colon cancer by DNA microarrays and correlation with histoclinical parameters

Gene expression profiling of colon cancer by DNA microarrays and correlation with histoclinical parameters

Basic transcription factor 3 (BTF3) regulates transcription of tumor-associated genes in pancreatic cancer cells

Protein-tyrosine Phosphatase PTPD1 Regulates Focal Adhesion Kinase Autophosphorylation and Cell Migration

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