BASP1 drives cisplatin resistance through LIN7A mediated epithelial-mesenchymal transition in OSCC. Bulk RNA seq
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Illumina NovaSeq 6000
ORGANISM(S): Homo sapiens
SUBMITTER: Dr Rupesh Dash
PROVIDER: E-MTAB-15141 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:In this study, we performed a CRISPR-based kinome screening in multiple cancer cell lines and identified Never In Mitosis Gene-A Related Kinase-9 (NEK9) as a major player of Docetaxel resistance in OSCC, prostate, and pancreatic cancer lines. We wanted to perform RNA sequencing to understand the possible mechanistic reason for drug sensitization.
2025-10-01 | E-MTAB-14795 | biostudies-arrayexpress
Project description:This study aims to identify combination treatments capable of inducing improved IO responses in lung tumours and thus, help guide decisions on the next combination arms for the HUDSON trial (post-IO). For that purpose, a lung tumour GEMM model was treated with either vehicle, PD-L1, ATR, ATR/PD-L1; Cisplatin/PD-L1/Ctla4 or VEGFR/PD-L1 and tumours collected for transcriptional profiling.
2024-01-29 | E-MTAB-13704 | biostudies-arrayexpress
Project description:UPF1 is a multi-domain RNA helicase that constantly monitors the transcriptome by non-specifically binding to mRNAs, dissociating from non-target transcripts, and initiating degradation on selected target RNAs via multiple proposed pathways such as nonsense-mediated decay (NMD). NMD is a translation-coupled mechanism that targets mRNAs harboring a premature stop codon (PTC) for degradation, thereby serving as a quality control and gene regulatory pathway ensuring transcriptome integrity. The execution of NMD requires the phosphorylation of N- and C-terminal tails of the key NMD factor UPF1, which thereby serve as binding platforms for the degradation factors SMG5, SMG6 and SMG7. UPF1 phosphorylation is mediated by the kinase SMG1, which catalytic activity can be inhibited with the SMG1 inhibitor SMG1i, a small molecule that functions as an ATP-competitive inhibitor and binds to the active site of SMG1. We wanted to assess the transcriptome-wide expression changes upon inhibition of SMG1. To this end, we treated human foreskin fibroblast (HFF) and human umbilical vein endothelial cells (HUVEC) with 1 µM SMG1i inhibitor for 24h. As controls, cells were treated with DMSO for 24h.
2025-09-01 | E-MTAB-14755 | biostudies-arrayexpress
Project description:MCF7, T47D and CAMA-1 cell lines were treated with long-term (continuous) capivasertib to induce resistant cell-lines (T47D P1, MCF7 P1 and CAMA-1 P1). The naïve (or parental) cell lines had RNAseq sequencing at treatment with DMSO and treatment with capivasertib. Resistant cell lines had RNAseq sequencing at treatment with continuous capivasertib, removal of continuous capivasertib and treatment with DMSO and then re-treatment with capivasertib monotherapy. This gave 5 time points across the different 3 different cell lines.
2026-05-25 | E-MTAB-16414 | biostudies-arrayexpress
Project description:UPF1 is a multi-domain RNA helicase that constantly monitors the transcriptome by non-specifically binding to mRNAs, dissociating from non-target transcripts, and initiating degradation on selected target RNAs via multiple proposed pathways such as nonsense-mediated decay (NMD). NMD is a translation-coupled mechanism that targets mRNAs harboring a premature stop codon (PTC) for degradation, thereby serving as a quality control and gene regulatory pathway ensuring transcriptome integrity. The UPF1 gene is essential in cultured human cells and previous studies relied mostly on RNA interference to downregulate UPF1. Here we established an auxin-inducible UPF1 degron system in the human colorectal adenocarcinoma cell line HCT116 by first inserting the auxin receptor F-box protein-encoding AtAFB2-mCherry in the AAVS1 locus, followed by tagging UPF1 at the N-terminus or C-terminus with an V5-AID-tag (AID = miniIAA7 = AtIAA7 amino acids 37–104). With these cell lines we wanted to assess the transcriptome-wide expression changes upon rapid depletion of UPF1, estimate the effects of auxin treatment and compare N-terminal versus C-terminal tagging. To this end, depletion of UPF1 was induced with 500 µM indole-3-acetic acid (IAA) for various time periods (0-12h). As controls, the parental cell line (with AtAFB2-mCherry in the AAVS1 locus) or untreated cells were used.
2025-09-01 | E-MTAB-13839 | biostudies-arrayexpress
Project description:UPF1 is a multi-domain RNA helicase that constantly monitors the transcriptome by non-specifically binding to mRNAs, dissociating from non-target transcripts, and initiating degradation on selected target RNAs via multiple proposed pathways such as nonsense-mediated decay (NMD). NMD is a translation-coupled mechanism that targets mRNAs harboring a premature stop codon (PTC) for degradation, thereby serving as a quality control and gene regulatory pathway ensuring transcriptome integrity. The UPF1 gene is essential in cultured human cells and previous studies relied mostly on RNA interference to downregulate UPF1. Here we established an auxin-inducible UPF1 degron system in the human colorectal adenocarcinoma cell line HCT116 by first inserting the auxin receptor F-box protein-encoding AtAFB2-mCherry in the AAVS1 locus, followed by tagging UPF1 at the N-terminus with an V5-AID-tag (AID = miniIAA7 = AtIAA7 amino acids 37–104). Using SLAM-Seq and this cell line, we wanted to explore the time-resolved RNA stability changes upon rapid depletion of UPF1. To this end, depletion of UPF1 was induced with 500 µM indole-3-acetic acid (IAA) for various time periods (0h, 12h and 24h) and the cells were labeled with 200 µM 4-thiouridine (4SU) the last 2 hours before harvesting. As controls, the parental cell line (with AtAFB2-mCherry in the AAVS1 locus) or unlabeled cells were used.
2025-09-01 | E-MTAB-13836 | biostudies-arrayexpress
Project description:Through various approaches we demonstrate that SYCP1 is aberrantly re-expressed in tumor cells, where it actively promotes DNA damage repair, cell cycle progression, and malignant growth. SYCP1 binds chromatin at regulatory elements and directly controls transcriptional programs governing genome maintenance, including key effectors such as CCNB1, PCNA, RAD51C, and H2AX. Loss of SYCP1 impairs DNA repair kinetics, attenuates tumor cell proliferation and migration, and increases sensitivity to chemotherapeutics cisplatin and gemcitabine. Mechanistically, SYCP1 interfaces with chromatin remodeling complexes and transcription factors SP1 and SP2, modulating their genomic occupancy and facilitating oncogenic transcriptional outputs. Our findings illuminate a previously unrecognized moonlighting function of SYCP1 in somatic cancer cells and position it as a critical chromatin-associated regulator of genome stability. In the presented RNA-seq experiment, we aimed to identify the differentially expressed genes between samples of wild type MCF7 cells and the samples with CRISPR/Cas9-mediated SYCP1 gene KO.
2026-03-15 | E-MTAB-15849 | biostudies-arrayexpress
Project description:CRISPR-Cas9 delivery by AAV holds promise for gene therapy but faces critical barriers due to its potential immunogenicity and limited payload capacity. Here, we demonstrate genome engineering in postnatal mice using AAV-split-Cas9, a multi-functional platform customizable for genome-editing, transcriptional regulation, and other previously impracticable AAV-CRISPR-Cas9 applications. We identify crucial parameters that impact efficacy and clinical translation of our platform, including viral biodistribution, editing efficiencies in various organs, antigenicity, immunological reactions, and physiological outcomes. These results reveal that AAV-CRISPR-Cas9 evokes host responses with distinct cellular and molecular signatures, but unlike alternative delivery methods, does not induce detectable cellular damage in vivo. Our study provides a foundation for developing effective genome therapeutics mRNA-Seq from muscles (9 samples; 3 mice x 3 conditions) and lymph nodes (9 samples; 3 mice x 3 conditions).
2016-07-29 | E-GEOD-84534 | biostudies-arrayexpress
Project description:Background: Microorganisms are the major cause of food spoilage during storage, processing and distribution. Pseudomonas fluorescens is a typical spoilage bacterium that contributes to a large extent to the spoilage process of proteinaceous food. RpoS is considered an important global regulator involved in stress survival and virulence in many pathogens. Our previous work revealed that RpoS contributed to the spoilage activities of P. fluorescens by regulating resistance to different stress conditions, extracellular acylated homoserine lactone (AHL) levels, extracellular protease and total volatile basic nitrogen (TVB-N) production. However, RpoS-dependent genes in P. fluorescens remained undefined. Results: RNA-seq transcriptomics analysis combined with quantitative proteomics analysis basing on multiplexed isobaric tandem mass tag (TMT) labeling was performed for the P. fluorescens wild-type strain UK4 and its derivative carrying a rpoS mutation. A total of 375 differentially expressed genes (DEGs) and 212 differentially expressed proteins (DEPs) were identified in these two backgrounds. The DGEs were further verified by qRT-PCR tests, and the genes directly regulated by RpoS were confirmed by 5’-RACE-PCR sequencing. The combining transcriptome and proteome analysis revealed a role of this regulator in several cellular processes, including polysaccharide metabolism, intracellular secretion and extracellular structures, cell well biogenesis, stress responses, ammonia and biogenic amine production, which may contribute to biofilm formation, stress resistance and spoilage activities of P. fluorescens. Moreover, in this work we indeed observed that RpoS contributed to the production of the macrocolony biofilm’s matrix.
2019-11-12 | PXD010845 | Pride
Project description:RNA-seq analysis was performed to understand the role of type I IFN response during SARS CoV-2 infection using transgenic mice. Each sample was collected from an individual C57BL/6J mouse. The total RNA was extracted from uninfected and SARS-CoV-2 infected mice lung tissue using RNeasy mini kit (QIAGEN #74104). The quantity of RNA was determined using Qubit RNA assay kit with Qubit 4.0 and the quality of RNA was tested using agarose gel electrophoresis and High Sensitivity Tape station Kit (Agilent 2200, #5067-5576, #5067-5577 and #5067-5578). After assessing the quality of RNA, ~900 ng of total RNA was taken for library preparation using NEBNext®Ultra™ II Directional RNA Library kit for Illumina (# E7760L) and NEBNext Poly (A) mRNA Magnetic Isolation Module (# E7490L) as per manufacturer's protocol. The prepared library was quantified using Qubit dsDNA assay kit (Invitrogen, Q32851) followed by quality check (QC) and fragment size distribution using a High Sensitivity Tape station Kit (Agilent 2200, #5067-5584 and #5067-5585). The library was sequenced using the HiSeq 4000 Illumina platform. The paired-end (PE) reads quality checks for each sample were carried out using FastQC v.0.11.5 (http://www.bioinformatics.babraham.ac.uk/projects/fastqc/). The adapter sequence was trimmed using the BBDuk version 37.58 version 37.58 and the alignment was performed using STAR v.2.5.3a with default parameters with human hg38 genome build, gencode v21 gtf 9GRCh38) from the gencode. The duplicates were discarded using Picard-2.9.4 (https://broadinstitute.github.io/picard/) from the aligned bam files and read counts were generated using featureCount v.1.5.3 from subread-1.5.3 package (https://bioinf.wehi.edu.au/) with Q = 10 for mapping quality. The count files were used as input for downstream differential gene expression analysis with DESeq2 version 1.14.1 9. The genes with read counts of ≤ 10 in any comparison were discarded followed by count transformation and statistical analysis using DESeq “R”. The “P” value were adjusted using the Benjamini and Hochberg multiple testing correction and the differentially expressed genes were identified (fold change of ≥1.5, P-value < 0.05). A unified non-redundant gene list was made for different comparisons and subjected to gene ontology (GO) analysis using the reactome database (https://reactome.org/). The top pathways (p < 0.05) were used for generating heat maps using Complexheatmap (Version 2.0.0) through unsupervised hierarchical clustering. The expression clusters were annotated based on enriched GO terms. Normalized gene expression was used to generate the boxplots with a median depicting the trends in the expression across the different conditions using ggplot2 [version 3.3.5]. The pathways analysis was performed using Metascape database (https://metascape.org/gp/index.html#/main/step1). The top pathways (p < 0.05) were taken for constructing bubble plots using ggplot2 [version 3.3.5].
2023-12-29 | E-MTAB-12681 | biostudies-arrayexpress