Homo sapiens
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: GSE20185
PROVIDER: PRJNA125677 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Analysis of genes regulated by cisplatin exposure, using non-tumourigenic keratinocytes to filter out genes regulated following cisplatin exposure that are unlikely to be involved in tumourigenesis. Results identify genes that may be important in mediating an increase in tumourigenic potential in cisplatin-resistant HNSCC cells.
2010-06-26 | GSE20185 | GEO
Project description:Cisplatin resistance is one of the main causes of treatment failure and death of head and neck squamous cell carcinoma (HNSCC). In order to better understand the mechanism of cisplatin resistance and formulate effective treatment strategies, we identified differentially expressed genes related to cisplatin resistance by RNA sequencing, RT-PCR and immunoblotting. CREB5 was selected as the most significantly up-regulated gene in cisplatin resistant cells. Gain- and loss-of-function experiments were performed to detect the effect of CREB5 on cisplatin resistance and mitochondrial apoptosis in HNSCC. Chromatin immunoprecipitation (ChIP) assay, dual-luciferase reporter assay, and immunoblotting experiments were performed to explore the underlying mechanisms of CREB5.
2022-07-07 | GSE202030 | GEO
Project description:Protein phosphorylation, a widely occurring and significant post-translational modification, is integral to various biological processes. We previously utilized a protein affinity probe to identify genes damaged by cisplatin, revealing that it inflicts substantial damage on protein kinase and protein phosphatase genes. In this study, we investigated cisplatin-induced alterations in the proteome and global phosphoproteome of A549 cells. Employing Fe-IMAC beads and tyrosine phosphorylation enrichment antibodies, we identified 6944 protein groups and 18,274 phosphorylation sites on 4,915 proteins across three biological replicates of both cisplatin-treated A549 cells and control cells. Among these, 730 tyrosine phosphorylation sites were identified—marking the most substantial discovery of such sites in A549 cells following cisplatin treatment. Bioinformatics analysis indicated that the proteins exhibiting significant phosphorylation level changes, which are predominantly involved in RNA processing, modification, transcription, translation, and the spliceosome. This suggests that cisplatin-induced damage to protein kinases and phosphatases may disrupt the normal function of these proteins, consequently impairing DNA replication, RNA translation, and shearing, ultimately culminating in tumor cell death. Moreover, we cross-referenced our proteomic data with our previously obtained cisplatin-damaged genes, observing that the majority of down-regulated proteins derived from cisplatin-induced gene damage.
2024-10-20 | PXD053902 | Pride
Project description:In order to improve therapy for head and neck squamous cell carcinoma (HNSCC), biomarkers associated with local and/or distant tumor relapses and cancer drug resistance are urgently needed. This study identified a potential biomarker, BAG-1 (Bcl-2 associated athanogene-1), that is implicated in HNSCC insensitive to cisplatin and tumor progression. Advanced HNSCC cells revealed resistant to cisplatin accompanied by increased expression of BAG-1 protein. siRNA knockdown of BAG-1 expression resulted in significant improvement of HNSCC sensitivity to cisplatin. BAG-1 expression enhanced stability of BCL-xL and conferred cisplatin resistant to the HNSCC cells. In addition, high levels of expression of phospho AKT, BAG-1, and BCL- xL were observed in advanced HNSCC compared to in that of primary HNSCC. Conclusion: Increased expression of BAG-1 was associated with cisplatin resistance and tumor progression in HNSCC patients and warrants further validation in larger independent studies. Over expression of BAG-1 may be a biomarker for cisplatin resistance in patients with primary or recurrent HNSCCs and targeting BAG-1 could be helpful in overcoming cisplatin resistance.
2017-10-04 | GSE102787 | GEO
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:Background: Oropharynx squamous cell carcinoma (OPSCC) is a subtype of HNSCC, arising from the base of tongue, lingual tonsil, tonsil, oropharynx, pharynx. The majority of OPSCC positive for HPV infection is associated with better prognosis, but a fraction of them, similarly to HPV-negative ones, is resistant to therapy and has poor prognosis. A deep molecular study of OPSCC is mandatory to identify either prognostic markers or targets for therapy, in particular in patients with worse prognosis. Methods: 14 HPV-positive and 15 HPV-negative Italian OPSCC (n=29) with complete clinical information and follow-up of more than 5 years were molecularly characterized by gene expression profiling and compared to three cohorts of OPSCC extracted from public HNSCC datasets. AKR1C3 emerged as robust marker overexpressed in HPV-negative OPSCC and in HPV-positive lesions with worse prognosis. Fadu and Cal-27 OPSCC cell lines were treated with AKR1C3 inhibitors, alone or in combination with Cisplatin. Results: Gene set enrichment analysis revealed that up-regulated genes in HPV-positive samples are involved in immune system, muscle related processes, response to stimuli, actin organization, tissue development and adhesion, while down-regulated genes participated in glutathione derivative biosynthetic and xenobiotic metabolic processes, hypoxia and oxidative stress. AKR1C3, coding for an enzyme involved in chemio-radioresistance, is in the top10 genes with higher upregulation in HPV-negative samples. Pre-treatment with a selective AKR1C3 inhibitor potentiated the effect of Cisplatin in cells with higher basal level of the enzyme. Conclusions: We identified a druggable target, AKR1C3, associated with survival in subgroups of OPSCC patients either positive or negative for HPV infection and to resistance to chemo-radiotherapy in HNSCC. Pretreatment of OPSCC cell lines expressing this enzyme with a selective AKR1C3 inhibitor is able to enhance Cisplatin efficacy.
2021-07-30 | GSE142583 | GEO
Project description:Treatment-related DNA hypermethylation may play a role in creating drug resistant phenotypes by inactivating genes that are required for cytotoxicity, but there have been no genome-wide studies to systematically investigate methylation of individual genes following exposure to chemotherapy. We used microarrays and a pharmacologic unmasking protocol in isogenic cisplatin-sensitive and -resistant cell lines to identify genes that were down-regulated in cisplatin-resistant cells and could be re-activated by the DNA methyltransferase inhibitor 5-Aza-2'-deoxycytidine (5-Aza-dC). We identified several hundred genes that were down-regulated in each resistant cell line. Of these, 30 genes were common to > 2 cell lines, and/or reported to be down-regulated in previous studies. siRNA knockdown of two candidate genes increased cell viability with cisplatin treatment in sensitive parental cell lines
2010-04-01 | GSE19397 | GEO
Project description:Cisplatin (DDP) is a widely used chemotherapeutic agent that induces apoptosis in various cancer cells, but its effects on endothelial cells such as HUVEC (Human Umbilical Vein Endothelial Cells) are less well understood. This study aims to explore the transcriptional response of HUVEC cells to cisplatin treatment. RNA-seq analysis was performed to identify differentially expressed genes following cisplatin stimulation, providing insights into the molecular mechanisms underlying the cellular response to chemotherapy in endothelial cells. The results highlight key pathways and genes involved in the stress response, apoptosis, and cellular survival in HUVEC cells upon cisplatin treatment.
2025-07-01 | GSE275662 | GEO
Project description:Cisplatin (DDP) is a widely used chemotherapeutic agent that induces apoptosis in various cancer cells, but its effects on endothelial cells such as HMEC-1 (Human Microvascular Endothelial Cell line-1) are less well understood. This study aims to explore the transcriptional response of HMEC-1 to cisplatin treatment. RNA-seq analysis was performed to identify differentially expressed genes following cisplatin stimulation, providing insights into the molecular mechanisms underlying the cellular response to chemotherapy in endothelial cells. The results highlight key pathways and genes involved in the stress response, apoptosis, and cellular survival in HMEC-1 cells upon cisplatin treatment.
2025-07-01 | GSE275667 | GEO
Project description:Platinum-based chemotherapy remains the cornerstone of treatment for most people with non-small cell lung cancer (NSCLC), either as adjuvant therapy in combination with a second cytotoxic agent or in combination with immunotherapy. Resistance to therapy, either in the form of primary refractory disease or evolutionary resistance, remains a significant issue in the treatment of NSCLC. Hence, predictive biomarkers and novel combinational strategies are required to improve the effectiveness and durability of treatment response for people with NSCLC. The aim of this study was to identify novel biomarkers and/or druggable proteins from deregulated protein networks within non-oncogene driven disease that are involved in the cellular response to cisplatin. Following exposure of NSCLC cells to cisplatin, in vitro quantitative mass spectrometry was applied to identify altered protein response networks. A total of 65 proteins were significantly deregulated following cisplatin exposure. These proteins were assessed to determine if they are druggable targets using novel machine learning approaches and to identify whether these proteins might serve as prognosticators of platinum therapy. Our data demonstrate novel candidates and drug-like molecules warranting further investigation to improve response to platinum agents in NSCLC.
2021-06-15 | PXD024209 | panorama