Transcript profiling of normal and transformed buccal keratinocytes
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE7862 | GEO | 2007/08/21
SECONDARY ACCESSION(S): PRJNA100001
REPOSITORIES: GEO
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Project description:Normal and two transformed buccal keratinocyte lines were cultured under a standardized condition to explore mechanisms of carcinogenesis and tumor marker expression at transcript and protein level. An approach combining three bioinformatic programs allowed coupling of abundant proteins and large-scale transcript data to low-abundance transcriptional regulators. The analysis identified previously proposed, and suggested novel, protein biomarkers, Gene Ontology categories and molecular networks including functionally impaired key regulator genes for buccal/oral carcinoma. Experiment Overall Design: Analysis of differential expression in two transformed buccal keratinocyte lines (SVpgC2a and SqCC/Y1) relative to normal buccal keratinocytes. Both normal and transformed cells were cultured under a standardized serum-free condition. Experiment Overall Design: Two replicates for all cell types were included.
2008-06-15 | E-GEOD-7862 | biostudies-arrayexpress
Project description:The current study analyzed a unique, serum-free medium derived tongue squamous cell carcinoma (TSCC) line termed LK0412 relative to the normal state to elucidate biomarkers at the protein and transcript level. A bioinformatics approach using Gene Ontology categories, gene networks and signature evaluation was applied to combine the protein and transcript data for identification of various gene signatures. The generated signatures were further assessed in public available data sets from normal and tumor tongue tissues. The analysis identified a novel gene signature that may improve the diagnosis and treatment of TSCC. Analysis of differential gene expression in LK0412 relative to the normal state. Both normal and LK0412 cells were cultured under a standardized serum-free condition.
2014-01-31 | E-GEOD-21866 | biostudies-arrayexpress
Project description:A tissue like buccal mucosa (from cheek swabs) would be an ideal sample material for rapid, easy collection for testing of biomarkers as an alternative to blood. A limited number of studies, primarily in the smoker/oral cancer literature, address this tissue's efficacy for quantitative PCR or microarray gene expression analysis. In this study both qPCR and microarray analyses were used to evaluate gene expression in buccal cells. An initial study comparing blood and buccal cells from the same individuals looked at relative amounts of four genes. The RNA isolated from buccal cells was degraded but was of sufficient quality to be used with RT-qPCR to detect expression of specific genes. Second, buccal cell RNA was used for microarray-based differential gene expression studies by comparing gene expression between smokers and nonsmokers. The isolation and amplification protocol allowed use of 150-fold less buccal cell RNA than had been reported previously with human microarrays. We report here the finding of a small number of significant gene expression differences between smokers and nonsmokers, using buccal cells as target material. Additionally, Gene Set Enrichment Analysis confirmed that these genes were changing expression in the same pattern as seen in an earlier buccal cell study performed by another group. Our results suggest that in spite of a high degree of RNA degradation, buccal cells from cheek mucosa could be used to detect differential gene expression between smokers and nonsmokers. However the RNA degradation, increase in sample variability and microarray failure rate show that buccal samples should be used with caution as source material in expression studies.
2010-03-01 | GSE16149 | GEO
Project description:The current study analyzed a unique, serum-free medium derived tongue squamous cell carcinoma (TSCC) line termed LK0412 relative to the normal state to elucidate biomarkers at the protein and transcript level. A bioinformatics approach using Gene Ontology categories, gene networks and signature evaluation was applied to combine the protein and transcript data for identification of various gene signatures. The generated signatures were further assessed in public available data sets from normal and tumor tongue tissues. The analysis identified a novel gene signature that may improve the diagnosis and treatment of TSCC.
2014-01-31 | GSE21866 | GEO
Project description:A tissue like buccal mucosa (from cheek swabs) would be an ideal sample material for rapid, easy collection for testing of biomarkers as an alternative to blood. A limited number of studies, primarily in the smoker/oral cancer literature, address this tissue's efficacy for quantitative PCR or microarray gene expression analysis. In this study both qPCR and microarray analyses were used to evaluate gene expression in buccal cells. An initial study comparing blood and buccal cells from the same individuals looked at relative amounts of four genes. The RNA isolated from buccal cells was degraded but was of sufficient quality to be used with RT-qPCR to detect expression of specific genes. Second, buccal cell RNA was used for microarray-based differential gene expression studies by comparing gene expression between smokers and nonsmokers. The isolation and amplification protocol allowed use of 150-fold less buccal cell RNA than had been reported previously with human microarrays. We report here the finding of a small number of significant gene expression differences between smokers and nonsmokers, using buccal cells as target material. Additionally, Gene Set Enrichment Analysis confirmed that these genes were changing expression in the same pattern as seen in an earlier buccal cell study performed by another group. Our results suggest that in spite of a high degree of RNA degradation, buccal cells from cheek mucosa could be used to detect differential gene expression between smokers and nonsmokers. However the RNA degradation, increase in sample variability and microarray failure rate show that buccal samples should be used with caution as source material in expression studies. Samples were collected from eight subjects, four smokers (Sm)and four nonsmokers (NS). Each cheek was sampled creating an a and b sample for each subject which is reflected in the array name. All samples were isolated separately for total RNA. Each was hybridzed to microarrays to examine for differential gene expression between smokers and nonsmokers. There are 14 total samples in the main dataset (Set 2). One cheek sample failed in microarray analysis for two individuals, 08BCNS23 a and 08BCSm27 a, and so are not included here. A sample set (Set 1) was created which contains the four samples shown in this file. They represent repeated sampling of both cheeks for two individuals to test for reproducibility. There is a separate RMA file and metadata file (this file) for these data. These included samples 08BC11Sm a and b, a smoker, and 08BC12NSa and b a nonsmoker.
2010-03-07 | E-GEOD-16149 | biostudies-arrayexpress
Project description:The most experiments about buccal pouch mucosal cells were investigated in mice and hamster. In these studies we have used porcine buccal pouch mucosal cells cultured primarily in vitro to investigate the expression profile of new molecular markers of mucosal wounding, vascularization and proliferation. In this study, we demonstrated the gene expression profile of long time primary cultured porcine buccal pouch mucosal cells.
2018-04-05 | GSE112659 | GEO
Project description:Tumor promotion is strongly associated with inflammation and increased polyamine levels. Our understanding of relevant mechanisms responsible for arsenic-induced cancer remains limited. Previous studies suggest that arsenic targets and dysregulates stem cell populations that remain dormant in the skin until promoted to be recruited out of the bulge stem cell region, thus giving rise to skin tumors. In this study, we explored a possible mechanism by which increased keratinocyte polyamine biosynthesis promotes tumorsphere formation and invasiveness of arsenic-transformed HaCaT keratinocytes (As-HaCaT). Unlike parental HaCaT cells, As-HaCaT cells were tumorigenic in athymic nude mice, and the CD45negative epithelial tumor cells had enriched expression of Toll-Like Receptor 4 (TLR4), CD34 and CXCR4 as did As-HaCaT tumorsphere cultures compared to As-HaCaT monolayer cultures. Ornithine decarboxylase (ODC) overexpressing keratinocytes (Ker/ODC) release increased levels of the alarmin high mobility group box 1 (HMGB1). Ker/ODC conditioned medium (CM) stimulated As-HaCaT but not parental HaCaT tumorsphere formation, and this was inhibited by glycyrrhizin, an inhibitor of HMGB1, and by TAK242, an inhibitor of the HMGB1 receptor TLR4. Compared to parental HaCaT cells, As-HaCaT cells demonstrated greater invasiveness across a Matrigel-coated filter using either fibroblast CM or SDF-1α as chemoattractants. Addition of Ker/ODC CM or HMGB1 dramatically increased As-HaCaT invasiveness. Glycyrrhizin and TAK242 inhibited this Ker/ODC CM-stimulated invasion of As-HaCaT cells but not HaCaT cells. These results show that polyamine-dependent release of HMGB1 promotes the expansion of stem cell-like subpopulations in arsenic-transformed keratinocytes while also increasing their invasiveness, suggesting that polyamines may be a potential therapeutic target for the prevention and treatment of arsenic-initiated skin cancers.
| S-EPMC6735862 | biostudies-literature
Project description:Using the Infinium HM450 platform, we have performed a longitudinal study of DNA methylation at birth and age 18 months in DNA from buccal swabs from 10 monozygotic (MZ) and 5 dizygotic (DZ) twin pairs from the Peri/postnatal Epigenetic Twins Study (PETS) cohort.
2013-03-06 | GSE42700 | GEO
Project description:Oral mucosa of smokers is subject to cigarette smoke (CS)-related cytological, genomic, and transcriptional changes that could potentially lead to the development of mouth diseases. In order to further characterize CS effects, we took advantage of two human organotypic in vitro models of the buccal and gingival epithelia (MatTek(R)) that have been developed from the same donor (healthy, non-smoker) to reflect the in vivo situation. Both gingival and buccal organotypic cultures were exposed to fresh, diluted CS at the air-liquid interface in parallel and 4 times (one conventional reference cigarette 3R4F at a time, 1 h intervals, CS dilution with air: 0.46 L/min or 0.16 L/min resulting in CS concentrations of 19.7% and 40.7% (v/v) respectively. Gene expression was captured at time 0 h following the 4th exposure and after different post-exposure time points (4h, 24h, 48h) to investigate time- and concentration-dependent CS effect on both tissues. Other endpoints (e.g. cytotoxicity, pro-inflammatory marker release, cytochrome P450 (CYP) activity, immunohistology) were also measured for some time points. By using computational approaches and by capturing systems biology endpoints, various perturbations of biological processes (e.g. inflammation, cell proliferation, cellular stress) triggered by repeated exposure to CS were analyzed in both buccal and gingival in vitro models. We describe here for the first time the impact of whole CS exposure on human buccal and gingival organotypic in vitro models using various approaches combining systems biology, biological network models, computational methods and standard endpoints.
2014-08-30 | E-MTAB-2251 | biostudies-arrayexpress
Project description:Serum-driven responses, many of which are related to wound healing, are potentially deregulated in cancer development and associated genomic alterations might have prognostic value. The current study assessed fetal bovine serum-induced transcriptomic changes for clinical relevance in head and neck squamous cell carcinoma (HNSCC) using oral keratinocyte models otherwise routinely cultured without serum, including normal keratinocytes (NOK) and the transformed keratinocyte lines SVpgC2a, SqCC/Y1 and LK0412. Bioinformatics-driven analysis of gene expression implicated primarily serum-induced terminal differentiation in NOK including alterations in 99 genes, 13 gene ontology-categories and 6 molecular networks and involvement of 7 key regulator genes. Compared to NOK, the transformed lines expressed around 3-fold lower numbers of differently expressed transcripts, unique sets of gene ontologies, molecular networks and key regulator genes for each line, and consistent absence of terminal differentiation markers. Assessment of the complete in vitro/serum exposure-derived set of differentially expressed genes (totally 180 genes) relative a clinical, information-rich HNSCC data set identified 17 survival-associated genes of which only 12 had previous association to HNSCC. Multi-step validation of the survival-associated genes relative to several independent tumor data sets, including in the Human Gene Expression Map and Human Protein Atlas databases, confirmed novel association to HNSCC for genes COTL1 and INSIG1 and novel poor outcome prediction for the genes CUL4B and PDGFRL. The definition of normal and aberrant serum responses in keratinocyte models therefore coupled new genes to HNSCC including with relevance to prognosis. Analysis of gene expression changes in serum-exposed normal and transformed cells relative the respective un-exposed states. Significantly differentially expressed genes were next assessed by bioinformatics processing using Gene Ontology categories and network analyses. Findings were also validated relative independent HNSCC data sets as well as transcriptomics and proteomics databases.
2014-01-01 | E-GEOD-39376 | biostudies-arrayexpress