RRBP1 rewires Cisplatin resistance in Oral Squamous Cell Carcinoma by regulating YAP-1
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ABSTRACT:
PROVIDER: PRJEB40913 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR4703472_1.fastq.gz | Fastqsanger.gz | |||
| ERR4703472_2.fastq.gz | Fastqsanger.gz | |||
| ERR4703473_1.fastq.gz | Fastqsanger.gz | |||
| ERR4703473_2.fastq.gz | Fastqsanger.gz | |||
| ERR4703474_1.fastq.gz | Fastqsanger.gz |
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Project description:The RNA-seq library preparation was performed on H357 CisS at 0 month,H357 CisR at 4 months, and H357 CisR at 8 months whereas CisR represent Cisplatin drug resistance and CisS denote sensitive to Cisplatin. Additional, we also performed gene specific knockdown on H357CisR 8 months RRPB1 Sh. In experiment, We have added two independent biological replicates of each samples to understand the role of causative factor for cisplatin resistance at transcriptomic level. Total RNA isolated from above mentions experiment and 2 μg of RNA was used to prepared library. The mRNA was isolated through magnetic beads using mRNA isolation kit (PolyA mRNA isolation Module, NEB) followed by RNA-seq library preparation using mRNA library preparation kit (NEB) strictly following the vendor recommended protocol. After library preparation concentration of libraries was estimated using qubit 2.0 (Invitrogen) and the recommended fragmentation sizes were confirmed by Tapestation (Agilent).
2020-12-31 | E-MTAB-9697 | biostudies-arrayexpress
Project description:Identification of CMTM6 as a novel mediator of cisplatin resistance in oral squamous cell carcinoma
2020-01-07 | MSV000084761 | MassIVE
Project description:BackgroundChemoresistance is one of the major factors for treatment failure in OSCC. Identifying key resistance triggering molecules will be useful strategy for developing novel treatment methods.MethodsTo identify the causative factors of chemoresistance, we performed RNA sequencing and global proteomic profiling of human OSCC lines presenting with sensitive, early and late cisplatin-resistance patterns.ResultsFrom the common set of dysregulated genes from both the analysis, RRBP1 was identified to be upregulated in both early and late cisplatin-resistant cells with respect to the sensitive counterpart. Analysis of OSCC patient sample indicates that RRBP1 expression is upregulated in chemotherapy-non-responder tumours as compared to chemotherapy-responder tumours. Genetic (knockout) or pharmacological (Radezolid, represses expression of RRBP1) inhibition of RRBP1 restores cisplatin-mediated cell death in chemo-resistant OSCC. Mechanistically, RRBP1 regulates Yes-associated protein1 (YAP1), a key protein in the Hippo pathway to induce chemoresistance. The PDC xenograft data suggests that knockout of RRBP1 induces cisplatin-mediated cell death and facilitates a significant reduction of tumour burden.ConclusionOverall, our data suggests that (I) RRBP1 is a major driver of cisplatin-resistance in OSCC, (II) RRBP1 regulates YAP1 expression to mediate cisplatin-resistance, (III) Radezolid represses RRBP1 expression and (IV) targeting RRBP1 reverses cisplatin-induced chemoresistance in advanced OSCC.
| S-EPMC8184829 | biostudies-literature
Project description:Oral squamous cell carcinoma (OSCC) is a prevalent form of cancer that develops from the epithelium of the oral cavity. OSCC is on the rise worldwide, and death rates associated with the disease are particularly high. Despite progress in understanding of the mutational and expression landscape associated with OSCC, advances in deciphering these alterations for the development of therapeutic strategies have been limited. Further insight into the molecular cues that contribute to OSCC is therefore required. Here we show that the transcriptional regulators YAP (YAP1) and TAZ (WWTR1), which are key effectors of the Hippo pathway, drive pro-tumorigenic signals in OSCC. Regions of pre-malignant oral tissues exhibit aberrant nuclear YAP accumulation, suggesting that dysregulated YAP activity contributes to the onset of OSCC. Supporting this premise, we determined that nuclear YAP and TAZ activity drives OSCC cell proliferation, survival, and migration in vitro, and is required for OSCC tumor growth and metastasis in vivo. Global gene expression profiles associated with YAP and TAZ knockdown revealed changes in the control of gene expression implicated in pro-tumorigenic signaling, including those required for cell cycle progression and survival. Notably, the transcriptional signature regulated by YAP and TAZ significantly correlates with gene expression changes occurring in human OSCCs identified by The Cancer Genome Atlas (TCGA), emphasizing a central role for YAP and TAZ in OSCC biology. Expression profiling was conducted following the repression of the transcriptional regulators TAZ and YAP (YAP/TAZ) in human SCC2 oral cancer cells. Human SCC2 oral cancer cells were transfected with control siRNA, or siRNAs targeting TAZ, YAP, or YAP/TAZ for 48 hours. Total RNA from three independent experiments carried out on separate days was isolated and purified and the samples were then profiled on Affymetrix Human Gene 2.0 Chips at the Boston University Microarray Core. The expression profiles were processed and normalized using the Robust Multi-array Average (RMA) procedure (23) based on a custom Brainarray CDF (24). For each of the siRNA experiments, signatures of genes differentially expressed between treatment and corresponding siRNA control with an FDR q-value ?0.05 and a fold change ?2 were identified as either activated (up-regulated in control) or repressed (up-regulated in treatment). The overlap between the differentially expressed gene signatures was evaluated by Fisher test. Hierarchical gene and sample clustering was performed on the top 3000 genes with highest median absolute deviation (MAD; a robust version of the variance) across 12 samples, using “ward” as the agglomeration rule, and 1 minus Pearson correlation and Euclidean as the distance measures for genes and samples, respectively.
2015-05-26 | E-GEOD-66949 | biostudies-arrayexpress
Project description:Oral squamous cell carcinoma (OSCC) is a prevalent form of cancer that develops from the epithelium of the oral cavity. OSCC is on the rise worldwide, and death rates associated with the disease are particularly high. Despite progress in understanding of the mutational and expression landscape associated with OSCC, advances in deciphering these alterations for the development of therapeutic strategies have been limited. Further insight into the molecular cues that contribute to OSCC is therefore required. Here we show that the transcriptional regulators YAP (YAP1) and TAZ (WWTR1), which are key effectors of the Hippo pathway, drive pro-tumorigenic signals in OSCC. Regions of pre-malignant oral tissues exhibit aberrant nuclear YAP accumulation, suggesting that dysregulated YAP activity contributes to the onset of OSCC. Supporting this premise, we determined that nuclear YAP and TAZ activity drives OSCC cell proliferation, survival, and migration in vitro, and is required for OSCC tumor growth and metastasis in vivo. Global gene expression profiles associated with YAP and TAZ knockdown revealed changes in the control of gene expression implicated in pro-tumorigenic signaling, including those required for cell cycle progression and survival. Notably, the transcriptional signature regulated by YAP and TAZ significantly correlates with gene expression changes occurring in human OSCCs identified by The Cancer Genome Atlas (TCGA), emphasizing a central role for YAP and TAZ in OSCC biology. Expression profiling was conducted following the repression of the transcriptional regulators TAZ and YAP (YAP/TAZ) in human SCC2 oral cancer cells.
2015-05-26 | GSE66949 | GEO
Project description:Cisplatin is a commonly used platinum-based chemotherapeutic agent for oral squamous cell carcinoma (OSCC). However, cisplatin efficacy is limited by drug toxicity and the resistance capabilities of cancer cells. Reduced efficacy of anticancer therapy has been recently attributed to the presence of therapy-insensitive subpopulations in heterogeneous tumours, known as cancer stem-like cells (CSCs). CSCs comprise a tumour-forming subpopulation of cells that exhibit stem cell-like features, including the abilities to self-renew and turn into progenitor and differentiated cancer cell lineages, and enhanced therapeutic resistance capabilities, thus driving the continual growth and survival of tumours. Overall, this work was conducted to provide the transcriptomes of the OSCC cell lines with differing responses to cisplatin using a microarray analysis. The data may be analyzed alongside other similar datasets to explore the underlying cisplatin resistance mechanisms in OSCC.
2021-03-09 | GSE168424 | GEO
Project description:chemoresistance frequently leads to therapeutic failure in oral squamous cell carcinoma (OSCC). Recently, studies have reported that lncRNAs play active roles in regulation biological properties of cancer. To understand whether lncRNAs involve in regulating cisplatin sensitivity in TSCC, in this study, we profiled the expression of lncRNAs in two TSCC cell lines(CAL-27 and SCC-9) under cisplatin treatment paired untreated cell lines by LncRNA Array (ArrayStar V3.0).
2018-06-12 | GSE114929 | GEO
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: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:There is large variability among lung squamous cell carcinoma (SCC) patients in response to treatment with cisplatin based chemotherapy. LncRNAs is potentional a new type of predictive marker that can identify subgroups of patients who benefit from chemotherapy and it will have great value for treatment guidance. Differentially expressed LncRNAs were identified using microarray profiling of tumors with partial response (PR) vs. with progressive disease (PD) from advanced lung SCC patients treated with cisplatin based chemotherapy and validated by quantitative real-time PCR (qPCR). Results: Compared with the PD samples, 953 lncRNAs were consistently overregulated and 749 lncRNAs
2015-05-18 | E-GEOD-59245 | biostudies-arrayexpress