New approaches to pathogenic gene function discovery with human squamous cell cervical carcinoma by gene ontology

Seo, Minjae; Bae, Su Mi; Kim, Yong-Wook; Hur, Soo Young; Ro, Duck Yeong; Lee, Joon Mo; Namkoong, Sung Eun; Kim, Chong Kook; Ahn, Woong Shick

doi:10.1016/j.ygyno.2004.11.032

Cited by 10 publications

(7 citation statements)

References 29 publications

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“…We showed that one of the new genes, APRIN/Pds5B (formerly AS3), was involved in proliferative arrest in vitro (Geck et al, 2000) and in vivo (Maffini et al, 2002). APRIN is a candidate tumor suppressor, its role in cancer pathways, its genomic losses or downregulation were detected in a variety of cancers and cancer cell lines (Geck et al, 2001), including esophageal (Harada et al, 2001;Zhang et al, 2008), head and neck (Reis et al, 2005), cervical (Seo et al, 2005), prostate (Murthy et al, 2005) and others.…”

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confidence: 96%

Loss of a cohesin-linked suppressor APRIN (Pds5b) disrupts stem cell programs in embryonal carcinoma: an emerging cohesin role in tumor suppression

et al. 2010

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Cohesins appear to have critical functions beyond mitotic cohesion. Our data on a cohesin-associated Pds5-paralog, APRIN, indicate a novel cohesin role in stem cell differentiation. APRIN/Pds5B is lost in many cancers and it is a putative tumor suppressor. Its mutations in the germ line, however, generate birth defects. We reasoned that as both cancer and birth defects share disrupted stem cell differentiation, the data suggest an APRIN/Pds5B cohesin function in stem cells. We used an embryonal carcinoma stem cell model and show here that (i) APRIN expression is precisely coordinated with stem cell differentiation; (ii) this coordination involves surface-contact and endocrine pathways; and (iii) APRIN/Pds5b coordination is critical in stem/progenitor exit decisions. APRIN knockdown disrupted Oct4, Nanog and SOX2 patterns, differentiation failed and the resulting immature proliferative cells did not progress beyond proneural progenitor phase. Furthermore, the phenotype-blocked progenitor exit (Mash-1 þ ); failed E-cadherin exit (E-Cadh low þ ); incomplete N-cadherin transition (N-Cadh low þ ); retained proliferative capacity (c-myc þ ); irregular stemness (SOX2 late þ þ ) and lost response to contact and hormonal cues-shares similarities with cancer-initiating cells. The data suggest novel APRIN/Pds5B-linked cohesin roles in stem/progenitor programs and a new mechanism in tumor suppression.

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confidence: 96%

Loss of a cohesin-linked suppressor APRIN (Pds5b) disrupts stem cell programs in embryonal carcinoma: an emerging cohesin role in tumor suppression

et al. 2010

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“…To further explore changes that mark the progression of HPV16-transformed cells toward malignancy, we compared the gene expression profiles of HKc/HPV16 to normal HKc and of HKc/DR to HKc/HPV16. The resulting gene lists were then compared with literature-derived lists of gene expression changes described in CIN, cervical cancer,16–28 as well as in other HPV-transformed cell lines 16,29–33…”

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confidence: 99%

“…15 To further explore changes that mark the progression of HPV16-transformed cells toward malignancy, we compared the gene expression profiles of HKc/HPV16 to normal HKc and of HKc/DR to HKc/HPV16. The resulting gene lists were then compared with literature-derived lists of gene expression changes described in CIN, cervical cancer, [16][17][18][19][20][21][22][23][24][25][26][27][28] as well as in other HPVtransformed cell lines. 16,[29][30][31][32][33] Material and methods Cell lines and cell culture conditions Normal HKc from neonatal foreskin were maintained in complete serum-free MCDB153-LB medium as previously described.…”

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confidence: 99%

Gene expression changes during HPV‐mediated carcinogenesis: A comparison between an in vitro cell model and cervical cancer

Wan

Miao

Quraishi

et al. 2008

Intl Journal of Cancer

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We used oligonucleotide microarrays to investigate gene expression changes associated with multi-step human papillomavirus type 16 (HPV16)-mediated carcinogenesis in vitro. Gene expression profiles in 4 early passage HPV16-immortalized human keratinocyte (HKc) lines derived from different donors were compared with their corresponding 4 late-passage, differentiation-resistant cell lines, and to 4 pools of normal HKc, each composed of 3 individual HKc strains, on Agilent 22 k human oligonucleotide microarrays. The resulting data were analyzed using a modified T-test coded in R to obtain lists of differentially expressed genes. Gene expression changes identified in this model system were then compared with gene expression changes described in published studies of cervical intraepithelial neoplasia (CIN) and cervical cancer. Common genes in these lists were further studied by cluster analysis. Genes whose expression changed in the same direction as in CIN or cervical cancer (concordant) at late stages of HPV16-mediated transformation in vitro formed one major cluster, while those that changed in the opposite direction (discordant) formed a second major cluster. Further annotation found that many discordant expression changes involved gene products with an extracellular localization. Two novel genes were selected for further study: overexpression of SIX1 and GDF15, observed during in vitro progression in our model system, was confirmed in tissue arrays of cervical cancer. These microarray-based studies show that our in vitro model system reflects many cellular and molecular alterations characteristic of cervical cancer, and identified SIX1 and GDF15 as 2 novel potential biomarkers of cervical cancer progression.

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“…It has been developed to manage the overwhelming mass of current biological data from a computational perspective and become a standard tool to annotate gene products for various databases [32], [33]. Accordingly, GO annotation has been being used for diverse sequence-based prediction tasks, such as analyzing the pathogenic gene function with human squamous cell cervical carcinoma [34], mapping molecular responses to xenoestrogens [35], predicting the enzymatic attribute of proteins [36], predicting the transcription factor DNA binding preference [37], and predicting the eukaryotic protein subcellular localization [38]. In particular, the growth of Gene Ontology databases has increased the effectiveness of GO-based features [39].…”

Section: Methodsmentioning

confidence: 99%

An Ensemble Classifier for Eukaryotic Protein Subcellular Location Prediction Using Gene Ontology Categories and Amino Acid Hydrophobicity

Zhang

Zou

et al. 2012

PLoS ONE

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With the rapid increase of protein sequences in the post-genomic age, it is challenging to develop accurate and automated methods for reliably and quickly predicting their subcellular localizations. Till now, many efforts have been tried, but most of which used only a single algorithm. In this paper, we proposed an ensemble classifier of KNN (k-nearest neighbor) and SVM (support vector machine) algorithms to predict the subcellular localization of eukaryotic proteins based on a voting system. The overall prediction accuracies by the one-versus-one strategy are 78.17%, 89.94% and 75.55% for three benchmark datasets of eukaryotic proteins. The improved prediction accuracies reveal that GO annotations and hydrophobicity of amino acids help to predict subcellular locations of eukaryotic proteins.

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New approaches to pathogenic gene function discovery with human squamous cell cervical carcinoma by gene ontology

Cited by 10 publications

References 29 publications

Loss of a cohesin-linked suppressor APRIN (Pds5b) disrupts stem cell programs in embryonal carcinoma: an emerging cohesin role in tumor suppression

Loss of a cohesin-linked suppressor APRIN (Pds5b) disrupts stem cell programs in embryonal carcinoma: an emerging cohesin role in tumor suppression

Gene expression changes during HPV‐mediated carcinogenesis: A comparison between an in vitro cell model and cervical cancer

An Ensemble Classifier for Eukaryotic Protein Subcellular Location Prediction Using Gene Ontology Categories and Amino Acid Hydrophobicity

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