The RNA-seq study of CCL20 in OSCC cell line
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1035051 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26641883_1.fastq.gz | Fastqsanger.gz | |||
| SRR26641883_2.fastq.gz | Fastqsanger.gz | |||
| SRR26641884_1.fastq.gz | Fastqsanger.gz | |||
| SRR26641884_2.fastq.gz | Fastqsanger.gz | |||
| SRR26641885_1.fastq.gz | Fastqsanger.gz |
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Project description:This study aimed to explore the underlying molecular mechanism of CCL20 in OSCC progression.
2025-06-03 | GSE246882 | GEO
Project description:Oral squamous cell carcinoma (OSCC) is a main reason of oral cancer mortality and morbidity. Cancer of oral cavity in central south Asia, ranks among third most common kinds of cancer. The discovery of candidate markers to differentiate normal from malignant cells in clinical diagnosis of OSCC would be of critical importance because this malignancy has poor prognosis. To improve the clinical outcome in OSCC patients, the present study was aimed at identifying robust candidate biomarkers for early OSCC diagnosis and to enhance understanding of the mechanisms of disease progression and pathogenesis. Of particular interest are proteins that can be found in tissue lysates of OSCC tumor vs normal adjacent mucosa samples and secreted in cell line Secretomes of HNSCC for non-invasive detection. We analysed 17 paired human malignant OSCC tissues and normal adjacent tissue in addition to secretomes of 9 HNSCC cell lines. The proteome dataset of OSCC and normal tissues consisted of 5,123 protein groups, including 299 proteins with strong differential expression (p-value <0.01, fold change barrier to ˃+2 and <-2, 205 upregulated and 94 down regulated) and 134 common proteins were also found out of total dataset of 4473 identified proteins of HNSCC cell line secretomes. Functional data analysis revealed that these differential proteins were significantly associated with multiple biological processes. Myogenesis, Fatty Acid Metabolism and KRAS Signaling DN were associated with the proteins downregulated in cancer tissues, while Protein Secretion, Unfolded Protein Response, Spliceosomal complex assembly, Protein localization to endosome and Interferon Gamma Response were enriched in the set of upregulated proteins and these regulated proteins may be classically or non-classically secreted. Furthermore, we found differential enrichment of Creb3L1, ESRRA, YY, ELF2, STAT1 and XBP transcription factors potentially regulating these major pathways.
2022-04-04 | PXD025701 | Pride
Project description:Oral squamous cell carcinoma (OSCC) is a main reason of oral cancer mortality and morbidity. Cancer of oral cavity in central south Asia, ranks among third most common kinds of cancer. The discovery of candidate markers to differentiate normal from malignant cells in clinical diagnosis of OSCC would be of critical importance because this malignancy has poor prognosis. To improve the clinical outcome in OSCC patients, the present study was aimed at identifying robust candidate biomarkers for early OSCC diagnosis and to enhance understanding of the mechanisms of disease progression and pathogenesis. Of particular interest are proteins that can be found in tissue lysates of OSCC tumor vs normal adjacent mucosa samples and secreted in cell line Secretomes of HNSCC for non-invasive detection. We analysed 17 paired human malignant OSCC tissues and normal adjacent tissue in addition to secretomes of 9 HNSCC cell lines. The proteome dataset of OSCC and normal tissues consisted of 5,123 protein groups, including 299 proteins with strong differential expression (p-value <0.01, fold change barrier to ?+2 and <-2, 205 upregulated and 94 down regulated) and 134 common proteins were also found out of total dataset of 4473 identified proteins of HNSCC cell line secretomes. Functional data analysis revealed that these differential proteins were significantly associated with multiple biological processes. Myogenesis, Fatty Acid Metabolism and KRAS Signaling DN were associated with the proteins downregulated in cancer tissues, while Protein Secretion, Unfolded Protein Response, Spliceosomal complex assembly, Protein localization to endosome and Interferon Gamma Response were enriched in the set of upregulated proteins and these regulated proteins may be classically or non-classically secreted. Furthermore, we found differential enrichment of Creb3L1, ESRRA, YY, ELF2, STAT1 and XBP transcription factors potentially regulating these major pathways.
2025-10-07 | MSV000099414 | MassIVE
Project description:Chemokine receptor CCR6 is a G-protein-coupled receptor that binds its high-affinity ligand, CCL20. Among the CD4+ T cells, Th17 and regulatory T cells express CCR6, which facilitates their migration in CCL20-enriched, inflamed tissue. Migration of CCR6+ T cells from secondary lymphoid tissues into inflamed tissues exposes them to a distinct metabolic microenvironment. What drives the metabolic adaptation of cells in these tissues and what contributes to their effector or regulatory function is not clearly understood. During colitis, increased gut production of CCL20 promotes the recruitment of these cells. We demonstrated that the intrinsic signaling of CCL20-CCR6 in CD4+ T cells promotes the differentiation of inflamatory Th1-like Th17 cells (T-bet+RORγt+) during colitis in both mouse models and humans. This signaling induces rapamycin-sensitive phosphorylation of PI3K, Akt, mTORC1, and STAT3 in a CCR6-dependent manner. RNA-seq and proteomics analysis revealed alterations in CCL20 during Th17 differentiation, affecting several metabolic pathways, including energy metabolism. CCL20 significantly increased glycolysis and inhibited oxidative phosphorylation, thereby driving the differentiation of pathogenic Th17 cells. Our findings suggest that alterations in CCR6-induced changes in Th17 metabolism offer an interesting therapeutic target for gut inflammation and autoimmunity.
2025-12-10 | PXD071790 | Pride
Project description:Hypoxic microenvironment plays important roles in the progression of solid tumors including oral squamous cell carcinoma (OSCC). Long noncoding RNAs (lncRNAs) have gained much attention in the past few years. However, it is not clear whether lncRNAs could regulate hypoxia-adaptation of OSCC, and which lncRNAs participate in this process. Using an lncRNA microarray, we analyzed the aberrant lncRNA expression profiles in OSCC tissues compared with paired normal oral mucosa as well as in hypoxic OSCC cells compared with normoxic OSCC cells. Our microarray also identified 942 lncRNAs that were up-regulated and 507 lncRNAs that were down-regulated in cells cultured under hypoxia compared with those cultured under normoxia (Fold Change >= 2.0, P-value <= 0.05). An OSCC cell line Cal-27 was cultured under either 20% O2 (normoxic) or 1% O2 (hypoxic) conditions. Three samples from each group were obtained for microarray study.
2016-07-26 | E-GEOD-84790 | biostudies-arrayexpress
Project description:Recent reports have revealed that EMT is involved in cancer invasion and progression including oral squamous cell carcinoma (OSCC). Previously, we have also studied on the association of p63 gene, a homolog of the p53 tumor suppressor gene, with EMT in OSCC cells. Furthermore, we also demonstrated that down-regulation of ΔNp63 accompanied with EMT and that re-expression of ΔNp63β by stable cDNA transfection in OSCC cell lines reverted the EMT phenotype. However, the detail mechanisms of ΔNp63β-mediated EMT remain to be unclear. Recent studies have shown that several microRNAs (miRNAs) are also involved in EMT process of human cancer by targeting EMT-related transcription factors. We thus sought to identify responsible miRNA associated with ΔNp63β-mediated EMT using miRNA microarray analyses.
2017-06-01 | GSE94047 | GEO
Project description:OSCC is associated with substantial mortality and morbidity. To identify potential biomarkers for the early detection of invasive OSCC, we compared the gene expressions of OSCC, oral dysplasia, and normal oral tissue from patients without oral cancer or preneoplastic oral lesions (controls). Results provided models of gene expression to distinguish OSCC from controls. RNA from 167 OSCC, 17 dysplasia and 45 normal oral tissues were extracted and hybridized to Affymetrix U133 2.0 Plus GeneChip arrays. The differentially expressed genes were identified using GenePlus software and the validation was done using RT-PCR, using independent internal and external datasets.
2011-07-21 | E-GEOD-30784 | biostudies-arrayexpress
Project description:In order to identify genes with differential gene expression or alternative splicing between the groups Normal and late stage OSCC (Stage III and IV), we study 16 hybridizations (6 normal; 10 late stage OSCC) on the HumanGene10ST array using mixed model analysis of variance. 1323 genes with significant gene expression differences between the groups and 357 genes with significant exon-group interaction (a symptom of alternative splicing) were found, including 129 genes with both gene and possible splicing differences (p<0.01). Contingency table analysis of the set of studied genes and a dataset of known pathways and gene classifications revealed that the set of alternatively spliced and expressed genes were found to be significantly over-represented in groups of the GOMolFn, GOProcess, GOCellLoc, and Pathway classes (p<0.01). Algorithm ANOVA study of 16 HumanGene10ST files. Factorial arrangment NORMALvs late stage OSCC samples
2014-09-30 | E-GEOD-56532 | biostudies-arrayexpress
Project description:Global gene expression comparisons between OSCC and normal oral mucosa samples have been performed in more than 20 cohorts since 2004. Pathologically relevant genes (and associated pathways) are hypothesized to be deregulated in all studies. A bioinformatics analysis was performed to identify recurrently deregulated genes and pathways in OSCC compared to normal oral mucosa. Among the 629 consistently deregulated genes, genes related to mitosis and cell division were highly enriched. These included the gene spindle and kinetochore-associated complex subunit 1 (SKA1), which was consistently upregulated in OSCC and associated with poor survival of OSCC patients. SKA1 is part of the outer kinetochore and is required for proper chromosome segregation. An oncogenic role of SKA1 has been established in other solid tumor entities; however, its role in OSCC and in the transformation of premalignant cells to overt cancer cells has not been extensively studied. To investigate its role, SKA1 was overexpressed in the human OSCC cell line CAL-33 and the oral premalignant leukoplakia cell line MSK-Leuk1, and knocked down in the human OSCC cell line SCC-25. SKA1 promoted proliferation and 2D colony formation, and reduced the proportion of cells in metaphase by shortening the duration of this phase in OSCC cells. In addition, SKA1 promoted cell migration as assessed by the scratch assay. Growth and 3D colony formation in Matrigel® were enhanced by SKA1 expression. Its overexpression increased, and its knockdown decreased the radioresistance of OSCC cells, while resistance to chemotherapy drugs used in OSCC treatment remained unchanged. In the premalignant cell line MSK-Leuk1, SKA1 increased proliferation, 2D colony formation, migration, and 3D colony formation. RNA-sequencing of CAL-33 and MSK-Leuk1 cells overexpressing SKA1 and control cells showed that SKA1 promoted the activation of different signaling pathways in the two cell lines. In OSCC cells, EMT and inflammatory response-related pathways were enriched upon SKA1 overexpression, while in premalignant cells, genes associated with proliferation and with SKA1 expression in OSCC patients were most enriched. In conclusion, SKA1 is a novel oncogene in OSCC that enhances proliferation, migration, and resistance to irradiation in OSCC and premalignant cells.
2025-04-14 | GSE262993 | GEO
Project description:OSCC is associated with substantial mortality and morbidity. To identify potential biomarkers for the early detection of invasive OSCC, we compared the gene expressions of OSCC, oral dysplasia, and normal oral tissue from patients without oral cancer or preneoplastic oral lesions (controls). Results provided models of gene expression to distinguish OSCC from controls.
2011-07-22 | GSE30784 | GEO