Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1177349 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31101723_1.fastq.gz | Fastqsanger.gz | |||
| SRR31101723_2.fastq.gz | Fastqsanger.gz | |||
| SRR31101724_1.fastq.gz | Fastqsanger.gz | |||
| SRR31101724_2.fastq.gz | Fastqsanger.gz | |||
| SRR31101725_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 24 |
Similar Datasets
Project description:Cisplatin-resistant gastric cancer (GC) occurs in patients with GC treated with cisplatin-based chemotherapy, which results in disease progression and early recurrence during the treatment. To understand the initiation and developmental mechanism underlying cisplatin-resistant GC, we developed cisplatin resistant SGC7901 cells (SGC7901/DDP) from the parental cells (SGC7901/S) by continuous exposure to increasing concentrations of cisplatin and subjected these two cell lines to RNA sequencing analysis.
2019-04-17 | GSE122130 | GEO
Project description:The plasticity of cancer stem cells (CSCs)/tumor-initiating cells (T-ICs) indicates that multiple CSC/T-IC subpopulations exist within a tumor and multiple oncogenic pathways collaborate to maintain the CSC/T-IC state. Here, we aimed to enrich for T-ICs from clinical ESCC tissues. A chemoresistant human esophageal squamous cell carcinoma (ESCC) patient-derived xenograft model was employed to identify miRNA(s) that contribute to ESCC aggressiveness. We used microarrays to demenstrate the microRNA expression underlying different pretreated conditions. NOG mice bearing subcutaneous tumor xenografts derived from clinical ESCC cells were intraperitoneally treated with CDDP or PBS twice weekly for three weeks. Tumor cells were then isolated and re-inoculated subcutaneously into NOG mice for the next round of treatment. In the 4th round of treatment, the volume of tumors in both CDDP- and PBS-treated groups were approximately the same, suggesting that the cells in CDDP-treated tumors were becoming resistant to CDDP. microRNA expression was measured by RNA extraction from cisplatin-treated tumors (EC-CR) or PBS-treated tumors(EC-UT) after 4 round of treatment,two microarrays were performed for each sample.
2016-06-16 | E-GEOD-83362 | biostudies-arrayexpress
Project description:We report the application of methyl-binding protein sequencing (MBD-seq) to global identify aberrant methylation between cisplatin sensitive and resistant ovarian cancer cell lines Detection of aberrant methylation states between cisplatin sensitive and resistant cell lines
2012-04-10 | E-GEOD-31418 | biostudies-arrayexpress
Project description:Cisplatin resistance is a major therapeutic challenge in advanced head and neck squamous cell carcinoma (HNSCC). Here, we aimed to investigate the key signaling pathway for cisplatin resistance in HNSCC cells. HNSCC cell lines that were sensitive (HN4 and HN30) or resistant (HN4/DDP and HN30/DDP) to cisplatin were used for this study. Moreover, the cisplatin-resistant human melanoma cell lines (A375/DDP) and human lung cancer cell lines (A549/DDP) have also been established. To identify the role of proteins in the acquisition of cisplatin resistance, we analyzed the abnormally expressed protein via protein mass spectrometry methods (isobaric tags for relative and absolute quantitation, iTRAQ) in cisplatin-sensitive and cisplatin-resistant cancer cells, and found that VN1R5 was highly expressed in cisplatin-resistant cells. Long noncoding RNA lnc-POP1-1 upregulated by VN1R5. To deeply investigate the mechanism by which lnc-POP1-1 affects cisplatin resistance in HNSCC cells, we used RNA pull-down assays followed by mass spectrometry to explore the putative RNA-binding proteins (RBPs) interacting with lnc-POP1-1.
2020-11-28 | PXD022799 |
Project description:Esophageal squamous cell carcinoma (ESCC) is a serious cancer with a poor prognosis and a high recurrence rate after chemotherapy, which is a major clinical challenge. To elucidate the molecular basis of chemotherapy (chemo)-resistance and develop methods to effectively eliminate chemo-resistant tumor clones, we established a cancer organoid model from 24 ESCC patients of various stages, ages, and treatments. These ESCCOs recapitulated most oncogenic mutations of primary ESCC tissues and had tumorigenic properties upon xenografting. Each organoid line differs in its responsiveness to 5-fluorouracil (5-FU) and cisplatin (CDDP), chemotherapeutic agents commonly used to treat ESCC patients, with 7 lines exhibiting potent chemo-resistance. Importantly, these chemo-resistant ESCCOs had enhanced expression of genes involved in antioxidant stress response pathways and increased chromatin accessibility of their genomic loci, compared to chemo-sensitive ESCCOs, and these genes became useful biomarkers that can stratify chemo-resistant ESCC in histopathological specimens.
2025-02-25 | GSE269447 | GEO
Project description:Cisplatin resistance is a problem in cancer treatment. Using DNA microarray, we detected differentially expressed genes in cisplatin-resistant cervix carcinoma HeLa cells compared to parental cells. Three cisplatin resistant cell lines were established by stepwise increasing cisplatin concentration. RNA from these resistant lines and its parental HeLa cells were labeled with Cy5 and Cy3. Equal amount of RNA from resistant cell line and HeLa were mixed and were hybridized to cDNA array. Signals were scanned and analyzed to find out the candidate genes involved in cisplatin resistant mechanism.
2010-05-06 | E-GEOD-15120 | biostudies-arrayexpress
Project description:Resistance to cisplatin is a key clinical concern in HPV-independent (HPV-) and HPV-associated (HPV+) head and neck cancer. Upregulation of DNA repair is known to contribute to cisplatin resistance and a major source of endogenous DNA damage are DNA/RNA hybrids, known as R-loops. Following creation of HPV+ and HPV- cisplatin resistant cell lines, RNA-Sequencing revealed alterations in the expression of known R-loop regulators. Resistant cells had elevated global R-loop levels and in HPV+ resistant cells there was a corresponding upregulation of the R-loop resolving protein, senataxin. Depletion of senataxin led to increased sensitivity to cisplatin, an increase in DNA damage and elevated R-loops at specific genomic loci. In summary, using an in vitro model of cisplatin resistance, we identified that senataxin modulates sensitivity to cisplatin through an R-loop mediated mechanism in HPV+ cells. R-loops may represent a potential therapeutic target and warrant further investigation.
2025-07-29 | GSE279046 | GEO
Project description:Chondrosarcoma is the second most common type of bone cancer. At present, the most effective clinical course of action is surgical resection. Cisplatin is the chemotherapeutic medication most widely used for the treatment of chondrosarcoma; however, its effectiveness is severely hampered by drug resistance. In the current study, we compared cisplatin-resistant chondrosarcoma SW1353 cells with their parental cells via RNA sequencing. Our analysis revealed that glutamine metabolism is highly activated in resistant cells but glucose metabolism is not. Amphiregulin (AR), a ligand of the epidermal growth factor receptor, enhances glutamine metabolism and supports cisplatin resistance in human chondrosarcoma by promoting NADPH production and inhibiting ROS accumulation. The MEK, ERK, and NrF2 signaling pathways were shown to regulate AR-mediated SLC1A5 and GLS expression as well as glutamine metabolism in cisplatin-resistant chondrosarcoma. The knockdown of AR expression in cisplatin-resistant chondrosarcoma cells was shown to reduce the expression of SLC1A5 and GLS in vivo. These results indicate that AR and glutamine metabolism are worth pursuing as therapeutic targets in dealing with cisplatin-resistant human chondrosarcoma.
2023-08-07 | GSE239911 | GEO