Effect of cisplatin in depletion MAGEA6 expression of esophageal cancer cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE229973 | GEO | 2023/05/01
REPOSITORIES: GEO
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Project description:To investigate mRNA expression difference in cisplatin chemo-sensitivity in esophageal squamous carcinoma patients. We performed gene expression profiling analysis using data obtained from RNA-seq of 6 different patients.
2023-05-01 | GSE229974 | GEO
Project description:A total of 20 KYSE human esophageal squamous cell carcinoma cell lines (KYSE-30, -140, -150, -170, -180, -200, -220, -350, -410, -450, -510, -520, -590, -770, -850, -890, -1170, -1190, -1250, and -2270) and a non-cancerous esophageal epithelial cell (HEEC-1)were kindly provided by Dr. Y. Shimada (Kyoto University, Kyoto, Japan). The KYSE cell lines were cultured in RPMI 1640 medium (Life Technologies, Inc., Grand Island, NY) containing 10% heat-inactivated fetal bovine serum (FBS; BioWhittaker, Verviers, Belgium) in a humidified atmosphere of 5% CO2 and maintained in continuous exponential growth by passage every 3 days. HEEC-1 cells were cultured in Keratinocyte SFM medium with growth supplement containing 2.5 mg EGF and 25 mg bovine pituitary extract in 500 mL liquid basal medium (GIBCO BRL, Rockville, MD) and expanded by passage twice in a week. The exponentially growing cultured cells (2 x 10^6) were collected after two-washings with PBS. Total RNA was prepared from the frozen cell pellets using QIAGEN RNeasy mini kit (QIAGEN, Inc., Valencia, CA), and mRNA was purified using MACS mRNA Isolation kit (Miltenyi Biotec, Bergisch Gladbach, Germany) according to the supplier’s protocols. RIKEN human 21K array containing 20,784 clones with positive and negative controls was used to analyze gene expression of 20 KYSE esophageal cancer cell lines using HEEC-1 as reference. The target DNAs used to construct human 21 K array were the glycerol stock of cDNA clones purchased from ResGen (Invitrogen Corporation, Carlsbad, CA)). One-microgram poly(A) RNAs from KYSE cells and the reference cells were labeled with Cy3-dCTP and Cy5-dCTP, respectively, by random-primed reverse transcription. Arrays were laser-scanned using ScanArray 5000TM confocal laser scanner (GSI Lumonics, Billerica, MA), and the images were analyzed using ScanAlyzeTM (Stanford University). All experiments were performed in duplicate (_1 & _2). Keywords: parallel sample
2005-12-31 | GSE2454 | GEO
Project description:A total of 20 KYSE human esophageal squamous cell carcinoma cell lines (KYSE-30, -140, -150, -170, -180, -200, -220, -350, -410, -450, -510, -520, -590, -770, -850, -890, -1170, -1190, -1250, and -2270) and a non-cancerous esophageal epithelial cell (HEEC-1)were kindly provided by Dr. Y. Shimada (Kyoto University, Kyoto, Japan). The KYSE cell lines were cultured in RPMI 1640 medium (Life Technologies, Inc., Grand Island, NY) containing 10% heat-inactivated fetal bovine serum (FBS; BioWhittaker, Verviers, Belgium) in a humidified atmosphere of 5% CO2 and maintained in continuous exponential growth by passage every 3 days. HEEC-1 cells were cultured in Keratinocyte SFM medium with growth supplement containing 2.5 mg EGF and 25 mg bovine pituitary extract in 500 mL liquid basal medium (GIBCO BRL, Rockville, MD) and expanded by passage twice in a week. The exponentially growing cultured cells (2 x 10^6) were collected after two-washings with PBS. Total RNA was prepared from the frozen cell pellets using QIAGEN RNeasy mini kit (QIAGEN, Inc., Valencia, CA), and mRNA was purified using MACS mRNA Isolation kit (Miltenyi Biotec, Bergisch Gladbach, Germany) according to the supplierâs protocols. RIKEN human 21K array containing 20,784 clones with positive and negative controls was used to analyze gene expression of 20 KYSE esophageal cancer cell lines using HEEC-1 as reference. The target DNAs used to construct human 21 K array were the glycerol stock of cDNA clones purchased from ResGen (Invitrogen Corporation, Carlsbad, CA)). One-microgram poly(A) RNAs from KYSE cells and the reference cells were labeled with Cy3-dCTP and Cy5-dCTP, respectively, by random-primed reverse transcription. Arrays were laser-scanned using ScanArray 5000TM confocal laser scanner (GSI Lumonics, Billerica, MA), and the images were analyzed using ScanAlyzeTM (Stanford University). All experiments were performed in duplicate (_1 & _2). To explore the genes responsible for chemosensitivity in cancer cells, expression profiles of various cancer cell lines were examined. Statistically comparing them with the chemosensitivity measured by in vitro MTT assay in each cell line, several candidate genes were selected and predicition models for anticancer efficacy were established using their expression levels.
2010-06-05 | E-GEOD-2454 | biostudies-arrayexpress
Project description:A total of 20 KYSE human esophageal squamous cell carcinoma cell lines (KYSE-30, -140, -150, -170, -180, -200, -220, -350, -410, -450, -510, -520, -590, -770, -850, -890, -1170, -1190, -1250, and -2270) were kindly provided by Dr. Y. Shimada (Kyoto University, Kyoto, Japan). The KYSE cell lines were cultured in RPMI 1640 medium (Life Technologies, Inc., Grand Island, NY) containing 10% heat-inactivated fetal bovine serum (FBS; BioWhittaker, Verviers, Belgium) in a humidified atmosphere of 5% CO2 and maintained in continuous exponential growth by passage every 3 days. The exponentially growing cultured cells (2 x 10^6) were collected after two-washings with PBS. Total RNA was prepared from the frozen cell pellets using QIAGEN RNeasy mini kit (QIAGEN, Inc., Valencia, CA). The quality of the RNA was checked using Agilent Technologies 2100 Bioanalyzer (Agilent, Palo Alto, CA). CodeLink Expression Bioarray System (Amersham Bioscience, Tokyo, Japan) was used according to the manufacturer’s protocol. Briefly, first-strand cDNA was generated from 1 µg of total RNA for each cell line using reverse transcriptase and a T7 primer, and then second-strand cDNA was produced using DNA polymerase mix and RNase H. cRNA was generated via an in vitro transcription reacrion using T7 RNA polymerase and biotin-11-UTP (Perkin Elmer, Boston, MA). After quantified by spectrometry and qualified using Agilent Technologies 2100 Bioanalyzer (Agilent), 10 µg of cRNA was fragmented and hybridized to a Uniset Human 20K I Bioarray containing 19,981 human probes with 108 positive and 300 negative bacterial control probes. After hybridization, the arrays were rinsed and labeled with Streptavidin-Cy5, scanned using Agilent DNA Microarray Scanner (Agilent), then analyzed with CodeLink Expression Analysis Software ver.2.3. Expression levels were normalized to the median expression value of the whole array spots except for the bacterial controls. Keywords: parallel sample
2005-12-31 | GSE2447 | GEO
Project description:Expression data from KYSE-150-shCtrl and KYSE-150-shCDKL3 cells
| PRJNA647917 | ENA
Project description:To reveal the modified gene regulatory elements including transcription factors and enhancers in esophageal squamous carcinoma cells (ESCC), we performed Assay for Transposase-Accessible Chromatin using sequencing (ATAC-seq) with two ESCC cell lines, i.e. KYSE-30 and KYSE-150, and a non-cancerous esophageal epithelial cell line, HET-1A. This data showed that hyper-accessible regions in ESCC cells contained genes related with cancer hallmarks including DNA replication and angiogenesis. Further motif analysis suggested that AP-1 family transcription factors bind the hyper-accessible regions in KYSE-30 cells as compared to those in HET-1A cells.
2021-11-04 | GSE162380 | GEO
Project description:A total of 20 KYSE human esophageal squamous cell carcinoma cell lines (KYSE-30, -140, -150, -170, -180, -200, -220, -350, -410, -450, -510, -520, -590, -770, -850, -890, -1170, -1190, -1250, and -2270) were kindly provided by Dr. Y. Shimada (Kyoto University, Kyoto, Japan). The KYSE cell lines were cultured in RPMI 1640 medium (Life Technologies, Inc., Grand Island, NY) containing 10% heat-inactivated fetal bovine serum (FBS; BioWhittaker, Verviers, Belgium) in a humidified atmosphere of 5% CO2 and maintained in continuous exponential growth by passage every 3 days. The exponentially growing cultured cells (2 x 10^6) were collected after two-washings with PBS. Total RNA was prepared from the frozen cell pellets using QIAGEN RNeasy mini kit (QIAGEN, Inc., Valencia, CA). The quality of the RNA was checked using Agilent Technologies 2100 Bioanalyzer (Agilent, Palo Alto, CA). CodeLink Expression Bioarray System (Amersham Bioscience, Tokyo, Japan) was used according to the manufacturerâs protocol. Briefly, first-strand cDNA was generated from 1 µg of total RNA for each cell line using reverse transcriptase and a T7 primer, and then second-strand cDNA was produced using DNA polymerase mix and RNase H. cRNA was generated via an in vitro transcription reacrion using T7 RNA polymerase and biotin-11-UTP (Perkin Elmer, Boston, MA). After quantified by spectrometry and qualified using Agilent Technologies 2100 Bioanalyzer (Agilent), 10 µg of cRNA was fragmented and hybridized to a Uniset Human 20K I Bioarray containing 19,981 human probes with 108 positive and 300 negative bacterial control probes. After hybridization, the arrays were rinsed and labeled with Streptavidin-Cy5, scanned using Agilent DNA Microarray Scanner (Agilent), then analyzed with CodeLink Expression Analysis Software ver.2.3. Expression levels were normalized to the median expression value of the whole array spots except for the bacterial controls. To explore the genes responsible for chemosensitivity in cancer cells, expression profiles of various cancer cell lines were examined. Statistically comparing them with the chemosensitivity measured by in vitro MTT assay in each cell line, several candidate genes were selected and predicition models for anticancer efficacy were established using their expression levels.
2010-06-05 | E-GEOD-2447 | biostudies-arrayexpress
Project description:Chemo-resistance to platinum such as cisplatin is critical in the treatment of ovarian cancer. Recent evidences have linked epithelial-mesenchymal transition (EMT) with the drug resistance as a contributing mechanism. The current study explored the connection between cellular responses to cisplatin with EMT in ovarian cancer. 46 ovarian carcinoma cell lines expression data with and without Cisplatin treatment.
2014-07-29 | E-GEOD-47856 | biostudies-arrayexpress
Project description:Radiotherapy and adjuvant cisplatin (DDP) chemotherapy are standard administrations applied in the treatment of NPC. However, molecular change and functions of DDP chemo-resistance in nasopharyngeal carcinoma are still poorly understood.
2019-08-01 | GSE135083 | GEO
Project description:The development of chemo-resistance has dramatically limited the clinical efficiency of platinum-based therapy. Although many resistant mechanisms have been demonstrated, genetic/molecular alterations responsible for drug resistance in the majority of clinical cases has not been identified. We analyzed three pairs of testicular germ cell tumor (TGCT) cell lines using Affymetrix expression microarrays to identify differential expressed genes. Then the expression of CCND1/CyclinD1, selected from the microarray analysis, was determined in cisplatin sensitive and resistance cancer samples including TGCTs, ovarian and prostate cancers by quantitative reverse transcription PCR analysis (qRT-PCR). Finally, we determined the gene knocked-down effect of CyclinD1. Expression microarray study revealed a limited number of differentially expressed genes across all three cell lines when comparing the parental and resistant cells. Among them, CyclinD1 was the most significantly differentially expressed gene. Importantly, we found that, in clinical TGCT samples, the overall expression level of cyclinD1 is higher in resistant cases compared to those sensitive samples (9/12 in the resistant group and only 3/8 in the sensitive group). We also found that cyclinD1 expressed dozens of fold higher in the resistant than in the sensitive ovarian cancer cell lines and dramatically overexpressed in prostate cancer. We re-sensitized the resistant cells by knocking-down cyclinD1. We demonstrated that deregulation of cyclinD1 is the major cause of TGCT cisplatin resistance and it may also be commonly involved in other human cancers. Combined cyclinD1 inhibition and cisplatin chemotherapy may be used clinically to treat the large number of cyclinD1 deregulated resistant tumors. RNA from three paired parental and cisplatin-resistant TGCT cell lines was extracted and analysed by Affymetrix gene expression microarray profiling (Human Genome U133 plus 2.0 arrays). Expression changes associated with the resistant phenotype were identified by comparing the three cisplatin-resistant derivatives to their parental counterparts.
2010-03-15 | E-GEOD-14231 | biostudies-arrayexpress