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FOXM1 in Early Human Squamous Cell Carcinoma Oncogenesis and it Is Enhanced by Nicotine during Malignant Transformation

ABSTRACT: Genome-wide SNP profilling for loss of heterozygosity (LOH) during FOXM1B-induced malignant transformation in a human premalignant oral keratinocyte line SVpgC2a. Keywords: oral cancer, keratinocytes, head and neck squamous cell carcinoma, FOXM1, genomic instability, SNP array, loss of heterozygosity, malignant transformation

ORGANISM(S): Homo sapiens

PROVIDER: GSE11782 | GEO | 2009/06/13

SECONDARY ACCESSION(S): PRJNA105975

REPOSITORIES: GEO

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Genotyping of human premalignant oral keratinocyte line SVpgC2a loss of heterozygosity (LOH) during FOXM1B-induced malignant transformation

Project description:Genome-wide SNP profilling for loss of heterozygosity (LOH) during FOXM1B-induced malignant transformation in a human premalignant oral keratinocyte line SVpgC2a. Experiment Overall Design: Eight FOXM1B-induced malignant clones (SVFN1-8) that grew in soft agar were grown as individual cell lines and gDNA harvested from each clone for SNP array analysis compared to wild-type non-transformed SVpgC2a as control to obtain loss of heterozygosity profiles.

2009-06-23 | E-GEOD-11782 | biostudies-arrayexpress

Upregulation of FOXM1 Induces Genomic Instability in Human Epidermal Keratinocytes

Project description:Genome-wide 10k SNP profiling of FOXM1B-transduced N/TERT and primary normal human epidermal keratinocytes (NHEK). The aim of this study was to study the cancer initiation role of UVB and FOXM1B upregulation in NHEK. Upregulation of FOXM1B alone (without UVB) was found to directly induce genomic instability in the form of copy number aberration (CNA) and low levels of loss of heterozygosity (LOH) in primary NHEK. The FOXM1B-induced CNA was found to be retained and accumulated in subsequent cell culture passages. UVB-exposure resulted in significant chromosomal LOH and CNA in N/TERT cells expressing FOXM1B but not in EGFP-expressing cells. This indicates that UVB corroborated with FOXM1B to recruit LOH and CNA which may predispose cell to malignant transformation. Collectively, these results indicate that aberrant upregulation of FOXM1B in skin keratinocytes following UVB exposure may be an early mechanism whereby cells acquire genomic changes required for oncogenesis. Keywords: Genome-wide SNP profiling for loss of heterozygosity (LOH) and copy number aberration (CNA), FOXM1, UVB, Keratinocytes, Basal cell carcinoma, genomic instability, carcinogenesis, squamous cell carcinoma.

2010-06-28 | GSE16937 | GEO

Upregulation of FOXM1 Induces Genomic Instability in Human Epidermal Keratinocytes

2010-07-29 | E-GEOD-16937 | biostudies-arrayexpress

FOXM1 Orchestrates a Global Methylation Signature that Mimics the Cancer Epigenome

Project description:Aberrant upregulation of a single oncogene FOXM1 in primary normal human oral epithelial cells orchestrated a cancer-like methylome landscape This study have identified a unique FOXM1-induced epigenetic signature which may have potentials as biomarkers for early oral cancer screening, diagnostic and/or therapeutic interventions Comparisons of primary human normal oral keratinocytes transduced with either EGFP (control) or FOXM1B and a head and neck squamous cell carcinoma cell line SCC15

2012-04-18 | E-GEOD-31767 | biostudies-arrayexpress

FoxM1, a critical regulator of oxidative stress during oncogenesis.

Project description:The transcription factor FoxM1 is over-expressed in most human malignancies. Although it is evident that FoxM1 has critical functions in tumour development and progression, the mechanisms by which FoxM1 participates in those processes are not understood. Here, we describe an essential role of FoxM1 in the regulation of oxidative stress that contributes to malignant transformation and tumour cell survival. We identify a negative feedback loop involving FoxM1 that regulates reactive oxygen species (ROS) in proliferating cells. We show that induction of FoxM1 by oncogenic Ras requires ROS. Elevated FoxM1, in turn, downregulates ROS levels by stimulating expression of ROS scavenger genes, such as MnSOD, catalase and PRDX3. FoxM1 depletion sensitizes cells to oxidative stress and increases oncogene-induced premature senescence. Moreover, tumour cells expressing activated AKT1 are 'addicted' to FoxM1, as they require continuous presence of FoxM1 for survival. Together, our results identify FoxM1 as a key regulator of ROS in dividing cells, and provide insights into the mechanism how tumour cells use FoxM1 to control oxidative stress to escape premature senescence and apoptosis.

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Gene expression changes associated with malignant transformation of oral potentially malignant disorders

Project description:Gene expression changes associated with malignant transformation of oral potentially malignant disorders

| PRJNA657049 | ENA

High malignant potential of betel quid-associated oral verrucous hyperplasia

Project description:Objectives. Oral verrucous hyperplasia (OVH) is commonly observed in the oral cavity of betel quid chewers that histologically display epithelial hyperplasia with or without dysplasia. Because of the high frequency of synchronous OVH adjacent to oral carcinomas, OVH is considered a potential malignant disorder, and studies of prognostic factors and genetic alterations are required. Materials and Methods. We conducted a follow-up study of 269 OVH patients at Chi-Mei Medical Center. A Kaplan-Meier analysis and Cox's proportional-hazards regression model were used to calculate the survival rate and prognostic factors of disease recurrence and transformation. Copy number variations (CNVs) were analyzed using a single-nucleotide polymorphism (SNP) array. Results. The 5-year disease-free and cancer-free survival rates of patients with OVH were 52% and 77%, respectively. Heavy betel quid (BQ) chewing (>20 nuts/day), the severity of oral submucosal fibrosis (OSF), and non-buccal and non-tongue lesions were high risk factors for malignant transformation, while dysplasia did not affect outcomes. A genetic analysis showed that OVH already possessed many CNVs present in oral squamous cell carcinoma (OSCC), and a bioinformatics analysis of CNV-associated genes revealed that the upregulation of CTTN, FOLR3, ORAOV1, PPFIA1, and RNF121 could help identify high-risk OVH patients. Conclusions. BQ-associated OVH has a high malignant potential, and more attention must be paid to OVH patients who have a heavy BQ chewing habit and advanced OSF, and whose tumor is located at non-buccal and non-tongue regions. The five CNV-associated genes can be used for early diagnosis and for predicting the prognosis.

2019-07-01 | GSE101761 | GEO

Gene expression profilings of normal human oral keratinocyte (HOK) and dysplastic oral keratinocyte cell line from a heavy smoker (DOK)

Project description:In our previous study, we identified global genetic and epigenetic aberrations in the tumors of oral squamous cell carcinoma (OSCC) patients who were habitual smokers. We hypothesized that cigarette smoke might play a role in oral malignant transformation. DOK cell line is a dysplasitc oral keratinocyte derived from a heavy smoker with OSCC. The differentially expressed genes between DOK and normal human oral keratinocytes (HOK) may provide important information about OSCC carcinogenesis mediated by cigarette smoking.

2015-12-31 | GSE54861 | GEO

Gene expression profilings of normal human oral keratinocyte (HOK) and dysplastic oral keratinocyte cell line from a heavy smoker (DOK)

2015-12-31 | E-GEOD-54861 | biostudies-arrayexpress

Transcriptome profiles of moderate dysplasia in oral mucosa associated with malignant conversion

Project description:Oral malignancies are among the top most deadly cancers in the world. Early diagnosis of oral premalignant and malignant lesions is essential for treatment decision-making and prognosis improvement. In this study, we systematically evaluated the gene expression patterns during the pathogenesis of oral moderate dysplasia. RNA sequencing detected 21556 genes in moderate dysplasia and paired normal tissues from three patients. Hierarchical clustering analysis revealed distinct gene expression patterns between the moderate dysplasia samples. 346 differentially expressed genes that may contribute to the pathogenesis of moderate dysplasia were identified. Among these genes, ISG15 and MAGEA family showed different transcription profiles that close related with the alterations of gene expression patterns in moderate dysplasia samples and paired normal tissues. We speculated that, as the potential marker to signal the risk of malignant transformation, ISG15 and MAGEA together with their close related misexpressed genes may involve in two different pathways during the malignant conversion from oral dysplasia to oral squamous cell carcinoma.

2017-06-28 | GSE72627 | GEO

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