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
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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: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: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: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: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
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. Analysis of 12 xenografts of human adenoid cystic carcinoma (ACC) along with 10 samples of ACC directly from humans. Note, that 12 of these samples are paired primary ACC & xenograft ACC from the same individual (6 pairs in total).
2011-05-03 | E-GEOD-28996 | biostudies-arrayexpress
Project description:Adenoid cystic carcinoma (ACC) is an extremely rare salivary gland tumor with a poor prognosis and needs attention on molecular mechanisms. Protein ubiquitination is an evolutionarily conserved post-translational modification (PTM) for substrates degradation and controls diverse cellular functions. The broad cellular function of ubiquitination network holds great promise to detect potential targets and identify respective receptors. Novel technologies are discovered for in-depth research and characterization of the precise and dynamic regulation of ubiquitylomics in multiple cellular processes during cancer initiation, progression and treatment. In the present study, 4D label-free quantitative techniques of ubiquitination proteomics were used and we identified a total of 4152 ubiquitination sites in 1993 proteins. We also performed a systematic bioinformatics analysis for differential modified proteins and peptides containing quantitative information through the comparation between oral ACC (OACC) tumor with adjacent normal tissues, as well as the identification of eight protein clusters with motif analysis. Our findings offered an important reference of potential biomarkers and effective therapeutic targets for ACC.
| S-EPMC8385350 | biostudies-literature
Project description:Adenoid cystic carcinoma (ACC) belongs to salivary gland malignancies commonly occurring in an oral cavity with a poor long-term prognosis. The potential biomarkers and cellular functions acting on local recurrences and distant metastases remain to be illustrated. Proteomics is the core content of precision medicine research, which provides accurate information for early detection of cancer, benign and malignant diagnosis, classification and personalized medication, efficacy monitoring, and prognosis judgment. To obtain a comprehensive regulation network and supply clues for the treatment of oral ACC (OACC), we utilized mass spectrometry-based quantitative proteomics to analyze the protein expression profile in paired tumor and adjacent normal tissues. We identified a total of 40,547 specific peptides and 4454 differentially expressed proteins (DEPs), in which HAPLN1 was the most upregulated protein and BPIFB1 was the most downregulated. Then, we annotated the functions and characteristics of DEPs in detail from the aspects of gene ontology, subcellular structural localization, KEGG, and protein domain to thoroughly understand the identified and quantified proteins. Glycosphingolipid biosynthesis and glycosaminoglycan degradation pathways showed the biggest difference according to KEGG analysis. Moreover, we confirmed 20 proteins from the ECM-receptor signaling pathway by a parallel reaction monitoring quantitative detection and 19 proteins were quantified. This study provides useful insights to analyze DEPs in OACC and guide in-depth thinking of the pathogenesis from a proteomics view for anticancer mechanisms and potential biomarkers.
| S-EPMC8319923 | biostudies-literature
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:Desmoglein 3 (Dsg3) is one of the desmosomal cadherins. Recent studies have reported that Dsg3 is abnormally expressed in oral squamous cell carcinoma (OSCC) and associated with tumor growth and poor survival. A role of Dsg3 in the progression of OSCC remains controversial, since both positive and negative effect on the cancer progression have been reported. Previously we have demonstrated that OSCC cells from the metastatic lymph nodes showed significantly higher DSG3 expression compared to those from the primary tumor of the same patients. Here we investigated the effect of Dsg3 expression on the growth of OSCC between anchorage-dependent (AD) and -independent (AID) conditions. Cell lines established from the primary tumor (P) and metastatic lymph nodes (LY) of three OSCC patients and two commercial OSCC cell lines were used for the experiments. Under AD conditions, Dsg3-low cell lines (Dsg3-low) had higher cell proliferation and migration ability than Dsg3-high cell lines (Dsg3-high) of the same patients. After transferred into AID conditions, all the cell lines except Dsg3-negative 7P showed increased Dsg3 expression by up to 50-fold, compared with AD conditions. Under AID conditions, all the patients showed higher cell proliferation ability in the Dsg3-high compared with Dsg3-low, which was marked contrast to AD conditions. Dsg3 knockdown under AD conditions increased the cell proliferation rate of all the cell lines except Dsg3-negative line. On the other hand, cell growth was not affected under AID conditions. These results suggested that Dsg3 may have two opposite effects on the growth of OSCC cells between AD and AID conditions, and that the involvement of molecules other than Dsg3 may also be important. Therefore, we investigated DEGs by Dsg3 knockdown under AD and AID conditions and their functions.
2024-12-24 | GSE275776 | GEO