Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA98793 | ENA |
REPOSITORIES: ENA
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2015-07-08 | E-GEOD-42874 | ExpressionAtlas
Project description:BACKGROUND: Basal cell carcinoma (BCC) is the most common form of human cancer. Though the genetic mutation and subsequent aberrant signaling role of the Hedgehog pathway in BCC development is understood, little is known about the downstream genetic mechanisms underlying BCC growth. The characterization of molecular events would improve our understanding of carcinogenesis and may define new therapeutic intervention opportunities. OBJECTIVE: To identify differential gene expression associated with tumorigenesis promotion and to define common signaling pathways significant in BCC survival and growth. METHODS: Microarray analysis, using a 21K expanded sequence verified cDNA set was performed on tissues obtained from previously untreated patients undergoing Mohs surgical resection (8 superficial BCC, 8 nodular BCC, 7 morphea form, 8 normal skin). Significantly differentially expressed genes were identified by analysis of microarray results in various data sets and subsequently screened for signaling pathway involvement. Selected genes were validated using real-time PCR analysis using an expanded set of 31 BCC samples. RESULTS: The global gene expression profiles in BCCs and normal skin were distinguishable by unpaired T test. 2429 genes were at least 1.5 fold differentially expressed between BCC (all morphological types) and normal skin (p < 0.01). Multiple singaling pathways were activated, but the hedgehog, WNT, MAPK and calcium signal transduction pathways predominated. CONCLUSION: Our findings may have important implications for understanding the pathogenesis of BCC and suggest targeting of the WNT and MAPK pathways with therapeutic intervention. Keywords: disease state analysis
2006-12-15 | GSE6520 | GEO
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Project description:Metformin is one of the first-line drugs for clinical treatment of type II diabetes, and recent studies have found that metformin can inhibit the development of multiple malignant tumors. When metformin is combined with chemotherapeutic drugs to treat head and neck squamous cell carcinoma（HNSCC）, it can effectively enhance the efficacy of chemotherapy. The aim of this study was to define the signaling pathways regulated by metformin in HNSCC, and the underlying mechanisms by which metformin sensitizes HNSCC chemotherapy. We used RNA sequencing (RNA-seq) to examine metformin regulated genes in the cal27, human tongue squamous carcinoma cell line, using RT-PCR to determine alterations in gene expression. Data from RNA-seq analysis showed that gene products involved in DNA replication, cell cycle, IL-17 signaling pathway, mismatch repair were all regulated by metformin. Our results suggest that metformin regulates multiple pathways associated with tumor growth and progression in HNSCC.
2022-07-03 | GSE207122 | GEO
Project description:We attempted to identify alterations in gene expression that occur during the progression from normal breast to ductal carcinoma in situ (DCIS) with the aim to elucidate significant genes and pathways underlying the premalignant transformation. To determine the expression changes that are common to multiple DCIS models (MCF10.DCIS, SUM102 and SUM225) and normal mammary epithelial cells (MCF10A), we grew the cells in three dimensional overlay culture with reconstituted basement membrane and used the extracted RNA for 76 cycles of deep sequencing (mRNA-Seq) using Illumina Genome Analyzer GAIIx. Analysis of mRNA-Seq results showed 295 consistently differentially expressed transcripts in DCIS models as compared to MCF10A. These differentially expressed genes are associated with a number of signaling pathways such as integrin, fibroblast growth factor and TGFM-CM-^_ signaling. Many differentially expressed transcripts in DCIS were found to be involved in cell-cell signaling, cell-cell adhesion and cell proliferation. We further investigated ALDH5A1 gene that encodes for the enzyme, aldehyde dehydrogenase 5A1, which is involved in glutamate metabolism. Further, inhibition of ALDH5A1 with different pharmacological drugs resulted in significant inhibition of cell growth and proliferation in the DCIS models. Four cell lines examined: normal mammary epithelial cell line (one sample) and three ductal carcinoma in situ cell lines (three samples). Each sample has two duplicates
2012-03-28 | E-GEOD-36863 | biostudies-arrayexpress
Project description:The potential therapeutic relevance of synthetic glycodendrimers was shown on animal subjects bearing colorectal carcinoma and melanoma. The application of glycodendrimers led to decreased tumor growth and prolonged survival time of the animals, accompanied by an enhancement of immune response. Comparison of mass spectra and biochemical analyses have indicated that the uptake of glycodendrimers by target cells resulted in changes of surface glycosylation. Moreover our research shows changes in membrane constitution. Recently our lab found changes in proliferation potential and expression of GnT-III and GnT-V in cancer cells in contrast to the peripheral blood mononuclear cells from healthy donors. As there are a sizable amount of enzymes involved in glycan metabolism and signaling pathways, the glyco-chip would be a very effective tool to determine which genes are involved in metabolism of these glycodendrimers. Our lab would like to develop expression profiles of cancer cells treated by glycodendrimers and a corresponding untreated control. For chip analyses we have chosen cell lines derived from chronic myeloid leukemia (K562), multiple myeloma (U266) and colon carcinoma (HT-29). There are untreated control samples and post glycodendrimers treatment samples from each cell line. All samples were produced and developed in triplicate for a total of 18 samples. The RNA was labeled and hybridized onto the GLYCOv3 array. .
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Project description:Multiple genes recruited from hormone pathways partition maize diterpenoid defences.
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