Ontology highlight
ABSTRACT:
PROVIDER: PRJNA663300 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12672372_1.fastq.gz | Fastqsanger.gz | |||
| SRR12672372_2.fastq.gz | Fastqsanger.gz | |||
| SRR12672373_1.fastq.gz | Fastqsanger.gz | |||
| SRR12672373_2.fastq.gz | Fastqsanger.gz | |||
| SRR12672374_1.fastq.gz | Fastqsanger.gz |
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Project description:Background: Despite extensive research efforts, glioblastoma (GBM) remains a deadly disease with poor prognosis. Although previous studies have identified various cell states within GBM tumors, the molecular mechanism underlying adaptive GBM cell plasticity induced by conventional therapy remains unclear. Methods: We used fluorescent reporters for proneural (PN) and mesenchymal (MES) subtypes to monitor GBM cell plasticity in real-time across multiple patient-derived cell lines. This approach revealed cells that concurrently expressed both proneural and mesenchymal markers. To investigate this unique hybrid population, we implemented a comprehensive methodological approach encompassing bulk and single-cell RNA sequencing, single-cell ChIP sequencing, nuclear proteomics, high-resolution imaging, orthotopic mouse models, clinical dataset analysis, and pharmacological and genetic techniques. This multifaceted strategy allowed us to gain functional and molecular insights into this distinct cellular population. Results: We showed that these hybrid cells are increased by conventional therapies, and are resistant to these therapies. At the molecular level, hybrid cells display significant alterations in chromatin structure and nuclear protein composition, elevated transcriptional activity, Myc activation, and improved transport between the nucleus and cytoplasm. Genetic and pharmaceutical inhibition of the nuclear import/export shuttling machinery, increased in hybrid cells, effectively suppressed adaptive GBM cell plasticity and hybrid identity, thereby enhancing the sensitivity of GBM cells to therapies. Conclusion: Our results indicate that GBM hybrid cells play a crucial role in chemoradiation resistance. The nuclear transport machinery presents a potential therapeutic target for hybrid cells, offering a way to counteract the typical resistance to treatment observed in GBM.
2025-07-09 | GSE256065 | GEO
Project description:European sculpins (Cottus) harbor an example of a recent hybrid speciation event, which entails the invasion of a new habitat by the hybrid species. We compare the transcriptomes of both parental species and the hybrid species to understand how they differ. F2 crosses between the parent species are compared to the hybrid species and its parent species to identify unique patterns of the hybrid species due to the initial hybridization process or respectively to other processes. See the accompanying publication (Czypionka et al. 2011.Transcriptome changes after genome wide admixture in invasive sculpins Molecular Ecology no doi yet) for more information. The transcriptome was compared between an invasive hybrid species of Cottus (Sieg population n = 8) and its parent species C.rhenanus and C.perifretum. Expression profiles of both parental populations were assessed by two independent replicate population (C.rhenanus: Broel and Naaf; C.perifretum Laarse Beek and Witte Nete; each population n = 8). The transcriptomes of F2 crosses between the populations of C.rhenanus and C.perifretum were assessed with for independent crosses with 4 biological replicates for each cross (n = 4 x 4 = 16). We used a custom design microarray with probes designed based on transcriptome sequencing. We used a newly developed calibration method to account for differences in individual probe binding behavior and to detect and remove probes unfit for analysis. Data stored as “normalized data” are normalized and quality filtered based on this new calibration method and normalized for interarray comparability by division by the 75%tile signal intensity for each array. Please refer to the accompanying publication (Czypionka et al. 2011.Transcriptome changes after genome wide admixture in invasive sculpins Molecular Ecology; no doi yet) for more information.
2012-03-26 | E-GEOD-36755 | biostudies-arrayexpress
Project description:Abstract Background Despite extensive research efforts, glioblastoma (GBM) remains a deadly disease with poor prognosis. Although previous studies have identified various cell states within GBM tumors, the molecular mechanism underlying adaptive GBM cell plasticity induced by conventional therapy remains unclear. Methods We used fluorescent reporters for proneural (PN) and mesenchymal (MES) subtypes to monitor GBM cell plasticity in real-time across multiple patient-derived cell lines. This approach revealed cells that concurrently expressed both proneural and mesenchymal markers. To investigate this unique hybrid population, we implemented a comprehensive methodological approach encompassing bulk and single-cell RNA sequencing, single-cell ChIP sequencing, nuclear proteomics, high-resolution imaging, orthotopic mouse models, clinical dataset analysis, and pharmacological and genetic techniques. This multifaceted strategy allowed us to gain functional and molecular insights into this distinct cellular population. Results We showed that these hybrid cells are increased by conventional therapies, and are resistant to these therapies. At the molecular level, hybrid cells display significant alterations in chromatin structure and nuclear protein composition, elevated transcriptional activity, Myc activation, and improved transport between the nucleus and cytoplasm. Genetic and pharmaceutical inhibition of the nuclear import/export shuttling machinery, increased in hybrid cells, effectively suppressed adaptive GBM cell plasticity and hybrid identity, thereby enhancing the sensitivity of GBM cells to therapies. Conclusion Our results indicate that GBM hybrid cells play a crucial role in chemoradiation resistance. The nuclear transport machinery presents a potential therapeutic target for hybrid cells, offering a way to counteract the typical resistance to treatment observed in GBM.
2025-07-09 | GSE256064 | GEO
Project description:Background: Despite extensive research efforts, glioblastoma (GBM) remains a deadly disease with poor prognosis. Although previous studies have identified various cell states within GBM tumors, the molecular mechanism underlying adaptive GBM cell plasticity induced by conventional therapy remains unclear. Methods: We used fluorescent reporters for proneural (PN) and mesenchymal (MES) subtypes to monitor GBM cell plasticity in real-time across multiple patient-derived cell lines. This approach revealed cells that concurrently expressed both proneural and mesenchymal markers. To investigate this unique hybrid population, we implemented a comprehensive methodological approach encompassing bulk and single-cell RNA sequencing, single-cell ChIP sequencing, nuclear proteomics, high-resolution imaging, orthotopic mouse models, clinical dataset analysis, and pharmacological and genetic techniques. This multifaceted strategy allowed us to gain functional and molecular insights into this distinct cellular population. Results: We showed that these hybrid cells are increased by conventional therapies, and are resistant to these therapies. At the molecular level, hybrid cells display significant alterations in chromatin structure and nuclear protein composition, elevated transcriptional activity, Myc activation, and improved transport between the nucleus and cytoplasm. Genetic and pharmaceutical inhibition of the nuclear import/export shuttling machinery, increased in hybrid cells, effectively suppressed adaptive GBM cell plasticity and hybrid identity, thereby enhancing the sensitivity of GBM cells to therapies. Conclusion: Our results indicate that GBM hybrid cells play a crucial role in chemoradiation resistance. The nuclear transport machinery presents a potential therapeutic target for hybrid cells, offering a way to counteract the typical resistance to treatment observed in GBM.
2025-07-09 | GSE256066 | GEO
Project description:We used small RNA-Seq to characterize heart non-coding RNAs in 85 inbred strains of mice from the Hybrid Mouse Diversity Panel (HMDP), a reference resource population for cardiovascular and metabolic traits.
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