Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Expression data from oral squamous cell carcinoma cell line Cal27 after lentivirus shIL-1beta transfection

ABSTRACT: Oral squamous cell carcinoma cell line Cal27 was transfected with lentiviral shIL-1beta or scrambled shRNA. We used microarrays to detail the global program of gene expression during this process. IL-1beta was identified as one of the key node genes in oral carainogenesis in our preveious in vitro study. This in vivo study was designed to confirm the role of IL-1 beta and explore some more detail about the evolvment of IL-1 in malignant transformation.

ORGANISM(S): Homo sapiens

SUBMITTER: Tong Wu

PROVIDER: E-GEOD-70301 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Modulation of IL-1β reprogrammes the tumor microenvironment to interrupt oral carcinogenesis.

Wu Tong T Hong Yun Y Jia Lihua L Wu Jie J Xia Juan J Wang Juan J Hu Qinchao Q Cheng Bin B

Scientific reports 20160201

Head and neck squamous cell carcinoma (HNSCC) development is a multistage process includes the normal, dysplasia and squamous cell carcinoma (SCC) stages. Recently, increasing evidence has suggested that the tumor microenvironment (TME) is an integral part of malignant transformation. Exploring certain key node genes in TME for future intervention in dysplasia to interrupt oral carcinogenesis was the primary goal of this research. To achieve this goal, systems biology approaches were first appli ...[more]

PMID: 26831400

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Project description:Epithelial ovarian cancer (EOC) accounts for 4% of all cancers in women and is the leading cause of death from gynecologic malignancies. It is well established that cancer invasion and metastasis still represent the major causes of the failure of cancer treatment. Previously, we identified the mannose receptor LY75 (DEC205/CD205) gene as notably hypomethylated in high-grade (HG) serous epithelial ovarian tumors, compared to normal ovarian tissues. LY75 has been identified as a putative antigen-uptake receptor, which is expressed abundantly on dendritic cells, which are specialist antigen presenting cells to T lymphocytes for the initiation of an immune response. The implication of LY75 in EOC tumorigenesis is currently unknown. Here we show that LY75 is strongly overexpressed in HG serous EOC tumors as compared to normal ovarian tissue. Importantly, shRNA-mediated LY75 knockout in the mesenchymal EOC cells (SKOV3) led to mesenchymal to epithelial transition (MET), associated with overexpression of epithelial markers E-cadherin and EPCAM and loss of expression of mesenchymal markers Fibronectin, N-cadherin Snail1 and Twist1. In addition, LY75 suppression significantly inhibited EOC cell migration and invasion in vitro. However, LY75 knockdown led to enhanced tumor cell dissemination and significantly increased lethality in vivo, in xenograft model of advanced peritoneal EOC. Thus, our findings indicate that LY75 could play an essential role in the mesenchymal-to-epithelial transition (MET) of EOC cells and support the hypothesis that, while epithelial-to-mesenchymal transition (EMT) enables the invasiveness of tumor cells, a MET-associated epithelial phenotype could be essential for their metastatic colonization. To better understand the molecular mechanisms of LY75 gene action in epithelial ovarian cancer (EOC), we employed the Agilent Whole Human Genome microarrays, containing ~ 44,000 genes to identify global gene expression changes upon LY75 suppression in SKOV3 EOC cells. We compared the gene expression of the previously selected shRNA-mediated LY75-knockdown clones sh-S3 and sh-S6 against the corresponding control (ctrl) clone. The microarray experiments were performed in duplicates, as two hybridizations were carried out for each of the LY75-suppressing cell clone against the corresponding control, using a fluorescent dye reversal (dye-swap) technique.

Dataset Information

Expression data from oral squamous cell carcinoma cell line Cal27 after lentivirus shIL-1beta transfection

Publications

Modulation of IL-1β reprogrammes the tumor microenvironment to interrupt oral carcinogenesis.

Similar Datasets

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