Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA237894 | ENA |
REPOSITORIES: ENA
Similar Datasets
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. Total RNA was collected from DOK and HOK cells followed by gene expression microarray analysis.
2015-12-31 | E-GEOD-54861 | biostudies-arrayexpress
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
Project description:To elucidate the potential role of small ncRNAs, such as piRNAs and miRNAs in oncogenesis of Oral squamous cell carcinoma (OSCC), we performed genome wide profiling in three human OSCC cell lines, H357 (tongue squamous cell carcinoma), KB (mouth cancer), Hep-2 (laryngeal cancer), and HOK (Normal human oral keratinocyte) using high-throughput RNA sequencing (RNA-Seq) of small RNAs. We discovered 4854 piRNAs in H357, 5184 in KB, 8340 in Hep-2, and 4735 in HOK, while miRNAs in H357, KB, Hep-2, and HOK were 1538, 1533, 1257, and 1468, respectively. This is the first study to identify both piRNAs and miRNAs in OSCCs, which will serve as a future resource for understanding the molecular mechanisms underlying the complex neoplastic events mediated by these small RNAs. Furthermore, these piRNAs and miRNAs have the potential to be used as biomarkers for OSCC.
2022-10-01 | GSE196674 | GEO
Project description:Purpose: Previously, we have reported the effectiveness of elemental diet (ED) Elental® against radiotherapy- or chemoradiotherapy- induced oral mucositis (Support Care Cancer 2016, Mol Clin Oncol 2019). However, administration of additional nutrition or ED in oral cancer patients might also provide extra nutrition for cancer cells, which could result in cancer development. At present, it is still unclear whether the beneficial effect of ED can be expected to surpass its possible harmful effect on oral cancer treatment. In the present study, we tried to clarify whether Elental® has different effects on human oral keratinocyte (HOK) cells compared to oral squamous cell carcinoma (OSCC) cells (HSC2). Method: Gene expression profiles of HOK cells and HSC2 cells treated with Elental® were generated by deep sequencing. Results: Whole transcriptome analysis data suggested that Elental® helped in the proliferation and survival of HOK through the induction of ERK. Moreover, Elental® added stress to HSC2 through the induction of endoplasmic reticulum stress response marker, BiP. Our results showed that Elental® might add stress to HSC2, and provide growth stimulation to HOK. Conclusion: Whole transcriptome analysis showed different gene expression profile between HOK cells and HSC2 cells treated with Elental®, suggesting that effects of Elental® might differ between normal oral cells and oral cancer cells.
2021-07-31 | GSE151420 | GEO
Project description:Cannabidiol (CBD) oral spray on murine oral ulcer significantly inhibited inflammation, relieved pain and accelerated healing process. To gain insight into transcriptional regulation of CBD on cells related to healing progress of oral ulcer, we performed RNA-Seq on the immortalized human oral keratinocyte HOK-16B cell lines stimulated with LPS and ATP, after 10μM CBD or vehicle excipient pretreatment.
2021-07-01 | GSE152088 | GEO
Project description:To investigate the effects of knockdown PGC1α on human dysplastic oral keratinocyte (DOK) cell proliferation, cell cycle, apoptosis, xenograft tumor, mitochondrial DNA (mtDNA), mitochondrial electron transport chain complexes (ECT), ROS, oxygen consumption rate (OCR), extracellular acidification rate (ECAR), and glucose uptake
2023-09-13 | GSE224317 | GEO
Project description:BACKGROUND: Cell lines have been developed for modeling cancer and cancer progression. The molecular background of these cell lines is often unknown to those using them to model disease behaviors. As molecular alterations are the ultimate drivers of cell phenotypes, having an understanding of the molecular make-up of these systems is critical for understanding the disease biology modeled. METHODS: Six immortalized normal, one immortalized dysplasia, one self-immortalized dysplasia, and two primary normal cell lines derived from oral tissues were analyzed for DNA copy number changes and changes in both mRNA and miRNA expression using SMRT-v.2 genome-wide tiling comparative genomic hybridization arrays, Agilent Whole Genome 4x44k expression arrays, and Exiqon V2.M-RT-PCR microRNA Human panels. RESULTS: DNA copy number alterations were detected in both normal and dysplastic immortalized cell lines—as well as in the single non-immortalized dysplastic cell line. These lines were found to have changes in expression of genes related to cell cycle control as well as alterations in miRNAs that are deregulated in clinical oral squamous cell carcinoma tissues. Immortal lines—whether normal or dysplastic—had increased disruption in expression relative to primary lines. All data are available as a public resource. CONCLUSIONS: Molecular profiling experiments have identified DNA,mRNA,andmiRNAalterations for a panel of normal and dysplastic oral tissue cell lines. These data are a valuable resource to those modeling diseases of the oral mucosa, and give insight into the selection of model cell lines and the interpretation of data from those lines. Total RNA from oral cancer cell lines were hybridized to Agilent 4x44k gene expression microarray
2014-07-10 | E-GEOD-59238 | biostudies-arrayexpress
Project description:micro-RNA in cancer-associated fibroblasts in oral squamous cell carcinoma vs. dysplasia-associated fibroblasts from dysplastic oral lesions vs. normal fibroblasts from normal oral mucosa from healthy individual.
2021-08-27 | GSE172287 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below. BACKGROUND: Cell lines have been developed for modeling cancer and cancer progression. The molecular background of these cell lines is often unknown to those using them to model disease behaviors. As molecular alterations are the ultimate drivers of cell phenotypes, having an understanding of the molecular make-up of these systems is critical for understanding the disease biology modeled. METHODS: Six immortalized normal, one immortalized dysplasia, one self-immortalized dysplasia, and two primary normal cell lines derived from oral tissues were analyzed for DNA copy number changes and changes in both mRNA and miRNA expression using SMRT-v.2 genome-wide tiling comparative genomic hybridization arrays, Agilent Whole Genome 4x44k expression arrays, and Exiqon V2.M-RT-PCR microRNA Human panels. RESULTS: DNA copy number alterations were detected in both normal and dysplastic immortalized cell lines?as well as in the single non-immortalized dysplastic cell line. These lines were found to have changes in expression of genes related to cell cycle control as well as alterations in miRNAs that are deregulated in clinical oral squamous cell carcinoma tissues. Immortal lines?whether normal or dysplastic?had increased disruption in expression relative to primary lines. All data are available as a public resource. CONCLUSIONS: Molecular profiling experiments have identified DNA,mRNA,andmiRNAalterations for a panel of normal and dysplastic oral tissue cell lines. These data are a valuable resource to those modeling diseases of the oral mucosa, and give insight into the selection of model cell lines and the interpretation of data from those lines.
2014-07-15 | GSE59407 | GEO
Project description:BACKGROUND: Cell lines have been developed for modeling cancer and cancer progression. The molecular background of these cell lines is often unknown to those using them to model disease behaviors. As molecular alterations are the ultimate drivers of cell phenotypes, having an understanding of the molecular make-up of these systems is critical for understanding the disease biology modeled. METHODS: Six immortalized normal, one immortalized dysplasia, one self-immortalized dysplasia, and two primary normal cell lines derived from oral tissues were analyzed for DNA copy number changes and changes in both mRNA and miRNA expression using SMRT-v.2 genome-wide tiling comparative genomic hybridization arrays, Agilent Whole Genome 4x44k expression arrays, and Exiqon V2.M-RT-PCR microRNA Human panels. RESULTS: DNA copy number alterations were detected in both normal and dysplastic immortalized cell lines—as well as in the single non-immortalized dysplastic cell line. These lines were found to have changes in expression of genes related to cell cycle control as well as alterations in miRNAs that are deregulated in clinical oral squamous cell carcinoma tissues. Immortal lines—whether normal or dysplastic—had increased disruption in expression relative to primary lines. All data are available as a public resource. CONCLUSIONS: Molecular profiling experiments have identified DNA,mRNA,andmiRNAalterations for a panel of normal and dysplastic oral tissue cell lines. These data are a valuable resource to those modeling diseases of the oral mucosa, and give insight into the selection of model cell lines and the interpretation of data from those lines.
2014-07-10 | GSE59238 | GEO