<HashMap><database>biostudies-arrayexpress</database><scores/><additional><omics_type>Unknown</omics_type><omics_type>Transcriptomics</omics_type><omics_type>Genomics</omics_type><omics_type>Proteomics</omics_type><submitter>Shilpee Dutt</submitter><instrument_platform>Illumina NovaSeq 6000</instrument_platform><study_type>RNA-seq of coding RNA</study_type><organism>Homo sapiens</organism><species>Homo sapiens</species><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/E-MTAB-13786</full_dataset_link><description>Glioblastoma is the most common, aggressive tumor of CNS, with a 5-year overall survival rate of 5%. The treatment is challenging due to its location and the inevitable recurrence in 80% of the cases. To understand the cause behind this recurrence, we established an in vitro radiation survival model that mimics clinical scenarios. GBM Parent (P) cells, after being given a lethal dose of radiation, undergo tremendous cell death but leave behind a small residual surviving population that shows senescence phenotype. These residual (RS) cells eventually reverse from senescence (End of senescence) and give rise to aggressive relapse (R). To find molecular players behind this reversal of senescence, we carried out RNA sequencing of GBM cell lines U87MG and SF268 at mentioned stages of senescence post-radiation treatment.</description><repository>biostudies-arrayexpress</repository><sample_protocol>Sequencing - Sequencing was performed to generate at least 60 million paired end reads per sample.</sample_protocol><sample_protocol>Nucleic Acid Extraction - Total RNA was isolated from cells using RNA Isoplus (Takara). Total mRNA was enriched from parent, RS, EOS and Relapse GBM samples and processed for library preparation.</sample_protocol><sample_protocol>Library Construction - Libraries were generated following the TruSeq RNA library protocol (Illumina). In summary, 4 μg of intact total RNA underwent mRNA purification through oligodT beads, and library preparation adhered to the manufacturer’s guidelines using the TruSeq RNA Sample Preparation Kit (Illumina).</sample_protocol><sample_protocol>Sample Collection - Parent GBM cells were grown to 70% confluency in vitro and subjected to their respective lethal doses of radiation U87MG (10Gy) and SF268 (8Gy). Cells were monitored for their SA-β galactosidase activity as gold standard for senescence detection and samples were harvested at the maximum SA-β gal positive population that is RS, when they lost senescence phenotype (EOS) and the regrown population thereof as Relapse (R).</sample_protocol><figure_sub>Organization</figure_sub><figure_sub>MINSEQE Score</figure_sub><figure_sub>Assays and Data</figure_sub><figure_sub>MAGE-TAB Files</figure_sub><pubmed_authors>Shilpee Dutt</pubmed_authors></additional><is_claimable>false</is_claimable><name>RNA seq from GBM cell lines and primary cultures after irradiation</name><description>Glioblastoma is the most common, aggressive tumor of CNS, with a 5-year overall survival rate of 5%. The treatment is challenging due to its location and the inevitable recurrence in 80% of the cases. To understand the cause behind this recurrence, we established an in vitro radiation survival model that mimics clinical scenarios. GBM Parent (P) cells, after being given a lethal dose of radiation, undergo tremendous cell death but leave behind a small residual surviving population that shows senescence phenotype. These residual (RS) cells eventually reverse from senescence (End of senescence) and give rise to aggressive relapse (R). To find molecular players behind this reversal of senescence, we carried out RNA sequencing of GBM cell lines U87MG and SF268 at mentioned stages of senescence post-radiation treatment.</description><dates><release>2026-02-08T00:00:00Z</release><modification>2026-02-08T02:02:31.398Z</modification><creation>2024-02-09T13:29:52.61Z</creation></dates><accession>E-MTAB-13786</accession><cross_references><ENA>ERP157317</ENA><EFO>EFO_0002944</EFO><EFO>EFO_0004170</EFO><EFO>EFO_0005518</EFO><EFO>EFO_0003738</EFO><EFO>EFO_0004184</EFO></cross_references></HashMap>