Gene expression comparison between two human cancer cell Lines: Oral squamous cell carcinoma SASL1m and adenoid cystic carcinoma ACC2
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE33171 | GEO | 2011/10/25
SECONDARY ACCESSION(S): PRJNA149217
REPOSITORIES: GEO
Similar Datasets
Project description:SASL1 is highly metastatic to lymph nodes. ACC2 is not metastatic. We compared gene expression on cultured cells to identify genes associated to metastatic spread patterns. SASL1m cells and ACC2 cells were cultured to confluence in 10 100mm dishes (5 per cell type). Total RNA was extracted (ISOGEN, Nippongene, Japan), purified by centrifugation, pooled and checked for quality (Eukaryote Total RNA Series II, Agilent, Sta Clara, USA) . Two samples of 2ɥg of Total RNA from SASL1m and ACC2 cells were labeled with biotin (3'IVT Labeling Kit, Affymetrix, USA) and hybridized (GeneAtlas Hybridization, Wash, and Stain Kit for 3' IVT Arrays, Affymetrix). The Microarray platform used was Affymetrix HG U219 Array Strip. The arrays were scanned in a GeneAtlas scanner controlled by GeneAtlas Software (Affymetrix, Sta. Clara, USA). No replicates were made. Genes were later filtered according to expression fold change (GeneSpring GX Software, Agilent, Sta Clara USA) and later organized in hypothetical networks (Ingenuity Pathway and Analysis Software, Ingenuity Systems, Redwood, USA). No control or reference samples were included. The expression of genes of interest was confirmed with qrt-PCR in the samples studied and four additional samples from cell cultures (Lightcycler, Roche, Switzerland).
2011-10-24 | E-GEOD-33171 | biostudies-arrayexpress
Project description:Background: Cervical lymph node metastasis is a potent prognostic factor in oral squamous cell carcinoma (OSCC). However, lymph nodes resected by sentinel node biopsy or neck dissection are usually diagnosed by examining only one or two sections of the maximal cut surface. Accurate diagnosis of the metastasis in lymph nodes is important but depends on a heavy workload of the pathologist. In this study, we have attempted to identify novel molecular markers to find the harboring cancer cells in the lymph node and establish rapid detection method. Methods: We determined the gene expression profiles of 7 metastatic lymph nodes from patients with OSCC and 1 normal lymph node and 5 salivary glands from non-cancerous patients by microarray analysis. We found the overexpression genes in all metastatic lymph nodes. Subsequently, we examined the expression of these genes in newly 23 metastatic lymph nodes and 9 normal lymph nodes by real-time quantitative RT-PCR (qRT-PCR) assay. Moreover, the rapid detection of lymph node metastasis by these genes was examined using the reverse transcription loop-mediated isothermal amplification (RT-LAMP) method. Result: Among the 4 genes identified by microarray analysis, annexin A8 (ANXA8) and desmoglein 3 (DSG3) were detected in all metastatic lymph nodes at a much higher level but not in normal lymph nodes at all by qRT-PCR. Furthermore, RT-LAMP method targeting ANXA8 rapidly detected almost lymph nodes with metastasis. Conclusions: ANXA8 could be a useful marker for detecting lymph node metastasis in OSCC.
2015-12-21 | GSE70604 | GEO
Project description:Background: Cervical lymph node metastasis is a potent prognostic factor in oral squamous cell carcinoma (OSCC). However, lymph nodes resected by sentinel node biopsy or neck dissection are usually diagnosed by examining only one or two sections of the maximal cut surface. Accurate diagnosis of the metastasis in lymph nodes is important but depends on a heavy workload of the pathologist. In this study, we have attempted to identify novel molecular markers to find the harboring cancer cells in the lymph node and establish rapid detection method. Methods: We determined the gene expression profiles of 7 metastatic lymph nodes from patients with OSCC and 1 normal lymph node and 5 salivary glands from non-cancerous patients by microarray analysis. We found the overexpression genes in all metastatic lymph nodes. Subsequently, we examined the expression of these genes in newly 23 metastatic lymph nodes and 9 normal lymph nodes by real-time quantitative RT-PCR (qRT-PCR) assay. Moreover, the rapid detection of lymph node metastasis by these genes was examined using the reverse transcription loop-mediated isothermal amplification (RT-LAMP) method. Result: Among the 4 genes identified by microarray analysis, annexin A8 (ANXA8) and desmoglein 3 (DSG3) were detected in all metastatic lymph nodes at a much higher level but not in normal lymph nodes at all by qRT-PCR. Furthermore, RT-LAMP method targeting ANXA8 rapidly detected almost lymph nodes with metastasis. Conclusions: ANXA8 could be a useful marker for detecting lymph node metastasis in OSCC. Using AB1700 system, we determined the gene expression profiles of lymph nodes with metastasis of OSCC. Normal lymph node and salivary gland tissues were used as control samples.
2015-12-21 | E-GEOD-70604 | biostudies-arrayexpress
Project description:Genome-wide methylation analysis was performed by methylated DNA immunoprecipitation-CGI microarray analysis. A pool of four cancer samples without lymph node metastasis, two pools of four cancer samples with lymph node metastasis, and three metastatic lymph nodes were prepared from the patients, and analyzed by MeDIP-CGI microarray.
2010-12-21 | E-GEOD-21238 | biostudies-arrayexpress
Project description:Background Oral squamous cell carcinoma (OSCC), an HPV-negative head and neck cancer, frequently metastasizes to the regional lymph nodes but only occasionally beyond. Initial phases of metastasis are associated with an epithelial–mesenchymal transition (EMT), while the consolidation phase is associated with mesenchymal–epithelial transition (MET). This dynamic is referred to as epithelial–mesenchymal plasticity (EMP). While it is known that EMP is essential for cancer cell invasion and metastatic spread, less is known about the heterogeneity of EMP states and even less about the heterogeneity between primary and metastatic lesions. Methods To assess both the heterogeneity of EMP states in OSCC cells and their effects on stromal cells, we performed single-cell RNA sequencing (scRNAseq) of 5 primary tumors, 9 matching metastatic and 5 tumor-free lymph nodes and re-analyzed publicly available scRNAseq data of 9 additional primary tumors. For examining the cell type composition, we performed bulk transcriptome sequencing. Protein expression of selected genes were confirmed by immunohistochemistry. Results From the 23 OSCC lesions, the single cell transcriptomes of a total of 7263 carcinoma cells were available for in-depth analyses. We initially focused on one lesion to avoid confounding inter-patient heterogeneity and identified OSCC cells expressing genes characteristic of different epithelial and partial EMT stages. RNA velocity and the increase in inferred copy number variations indicated a progressive trajectory towards epithelial differentiation in this metastatic lesion, i.e., cells likely underwent MET. Extension to all samples revealed a less stringent but essentially similar pattern. Interestingly, MET cells show increased activity of the EMT-activator ZEB1. Immunohistochemistry confirmed that ZEB1 was co-expressed with the epithelial marker cornifin B in individual tumor cells. The lack of E-cadherin mRNA expression suggests this is a partial MET. Within the tumor microenvironment we found immunomodulating fibroblasts that were maintained in primary and metastatic OSCC. Conclusions This study reveals that EMP enables different partial EMT and epithelial phenotypes of OSCC cells, which are endowed with capabilities essential for the different stages of the metastatic process, including maintenance of cellular integrity. During MET, ZEB1 appears to be functionally active, indicating a more complex role of ZEB1 than mere induction of EMT.
2023-04-24 | GSE195655 | GEO
Project description:SASL1 is highly metastatic to lymph nodes. ACC2 is not metastatic. We compared gene expression on cultured cells to identify genes associated to metastatic spread patterns. SASL1m cells and ACC2 cells were cultured to confluence in 10 100mm dishes (5 per cell type). Total RNA was extracted (ISOGEN, Nippongene, Japan), purified by centrifugation, pooled and checked for quality (Eukaryote Total RNA Series II, Agilent, Sta Clara, USA) . Two samples of 2ɥg of Total RNA from SASL1m and ACC2 cells were labeled with biotin (3'IVT Labeling Kit, Affymetrix, USA) and hybridized (GeneAtlas Hybridization, Wash, and Stain Kit for 3' IVT Arrays, Affymetrix). The Microarray platform used was Affymetrix HG U219 Array Strip. The arrays were scanned in a GeneAtlas scanner controlled by GeneAtlas Software (Affymetrix, Sta. Clara, USA). No replicates were made. Genes were later filtered according to expression fold change (GeneSpring GX Software, Agilent, Sta Clara USA) and later organized in hypothetical networks (Ingenuity Pathway and Analysis Software, Ingenuity Systems, Redwood, USA). No control or reference samples were included. The expression of genes of interest was confirmed with qrt-PCR in the samples studied and four additional samples from cell cultures (Lightcycler, Roche, Switzerland).
| S-ECPF-GEOD-33171 | biostudies-other
Project description:In this study, we investigated CNAs of 40 tumor samples from 25 patients, including 15 metastatic primary tumor (MPT), paired neck lymph-node metastasis (LNM) and 10 non-metastatic primary tumor (NMPT), by 44k oligonucleotide-based array comparative genomic hybridization (array CGH).
2013-09-08 | GSE36942 | GEO
Project description:Metastasis via the lymphatics is a major risk factor in squamous cell carcinoma of the oral cavity (OSCC). We sought to determine whether the presence of metastasis in the regional lymph node could be predicted by a gene expression signature of the primary tumor. A total of 18 OSCCs were characterized for gene expression by hybridizing RNA to Affymetrix U133A gene chips. Genes with differential expression were identified using a permutation technique and verified by quantitative RT-PCR and immunohistochemistry. A predictive rule was built using a support vector machine, and the accuracy of the rule was evaluated using crossvalidation on the original data set and prediction of an independent set of four patients. Metastatic primary tumors could be differentiated from nonmetastatic primary tumors by a signature gene set of 116 genes. This signature gene set correctly predicted the four independent patients as well as associating five lymph node metastases from the original patient set with the metastatic primary tumor group. We concluded that lymph node metastasis could be predicted by gene expression profiles of primary oral cavity squamous cell carcinomas. The presence of a gene expression signature for lymph node metastasis indicates that clinical testing to assess risk for lymph node metastasis should be possible.
2007-08-25 | E-GEOD-2280 | biostudies-arrayexpress
Project description:In this study, we investigated CNAs of 40 tumor samples from 25 patients, including 15 metastatic primary tumor (MPT), paired neck lymph-node metastasis (LNM) and 10 non-metastatic primary tumor (NMPT), by 44k oligonucleotide-based array comparative genomic hybridization (array CGH). 15 MPT vs 15 LNM, 10 NMPT vs 15 LNM
2013-09-08 | E-GEOD-36942 | biostudies-arrayexpress
Project description:Adenoid cystic carcinoma (ACC) is one of the most common malignancies that arise in the salivary glands, with an incidence of 4.5 per 1,000,000. It can also arise in glandular tissue closely related to salivary glands in the lacrimal gland, nasal passages and tracheobronchial tree, as well as in glands of the breast and vulva. At all of these sites, it is characterized by a distinctive histology of basaloid epithelial cells arranged in cribriform or tubular patterns, usually demonstrating abundant hyaline extracellular matrix secretion and some degree of myoepithelial differentiation. ACC is generally a slow-growing tumor characterized by a protracted clinical course, usually well over 5 years in duration, marked by regional recurrence, distant metastasis and/or spread along peripheral nerves. A recurrent chromosomal translocation, t(6;9)(q23;p21), has been identified in ACC, and recently it has been discovered that in a majority of ACC the MYB gene on chromosome 6 is fused to the 3’ terminus of the NFIB gene on chromosome 9, creating a fusion gene product resulting in increased MYB-related transcriptional activation. Recently it has been determined that most cell lines with attribution of ACC derivation are either contaminants of other cell lines or do not have the characteristic MYB-NFIB translocation. Also, there are no animal models of this histologically and genetically defined tumor type. To address the paucity of experimental and pre-clinical models systems of ACC, we have for several years been establishing xenograft tumor lines from clinical samples of ACC. We describe our experience with these models and their characterization here.
2011-05-03 | GSE28996 | GEO