Genome-wide gene expression prolifing post GNL3 knockdown in human neural progenitor cells
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ABSTRACT:
PROVIDER: PRJNA634131 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11819878_1.fastq.gz | Fastqsanger.gz | |||
| SRR11819878_2.fastq.gz | Fastqsanger.gz | |||
| SRR11819879_1.fastq.gz | Fastqsanger.gz | |||
| SRR11819879_2.fastq.gz | Fastqsanger.gz | |||
| SRR11819880_1.fastq.gz | Fastqsanger.gz |
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Project description:We used two siRNAs to knock down GNL3 in human neural progenitor cells which were derived from normal human induced pluripotent stem cells (ATCC, ACS-1011). GNL3 knockdown experiments were done in three biological replicates. Total RNA was extracted from GNL3 knockdown and control groups for RNA sequencing (Illumina Hiseq2000, paired-end 100 bp). Genes that affected by both siRNAs were considered differentially expressed genes between GNL3 knockdown and control groups (adjusted P value < 0.05). Using Gene Ontology and KEGG pathway analysis, we found that those differentially exrepssed genes were mainly related to immune response, response to cytokine, cell cycle, and p53 signaling pathway.
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Project description:The objective of the study was to examine changes in gene expression induced by CYP2E1 knockdown in neural progenitor cells.There were 6samples in total.Samples shs_1, shs_2, and shs_3 are the control group, and shCYP2E1_1, shCYP2E1_2, and shCYP2E1_3 are the CYP2E1 knockdown group.Neural progenitor cells were cultured in vitro from normal fetal brain tissue aborted at 21 weeks, infected with CYP2E1_shRNAs and CYP2E1_shRNA lentivirus respectively, and then differentiated and cultured for 4 days.The total RNA of each sample was extracted from the lentivirus infected, early differentiated human neural progenitor cells with TRIzol reagent.Then the RNA samples were processed for high throughput transcriptome sequencing on Illumina HiSeq 3000 platform.
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Project description:Genome-wide gene expression profiling post GNL3 knockdown in human neural progenitor cells
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Project description:DNA double-strand break (DSB) repair via homologous recombination (HR) is critical for maintaining genomic integrity and requires proper DNA end resection to generate ssDNA overhangs. Yet, how this critical step is regulated in cells remains to be understood. Here, we report that GNL3, a nucleolar GTP-binding protein, plays a critical role in HR repair via regulating DNA end resection dependently on its SUMOylation. Ectopic expression of wild-type, but not the SUMO-defective K196R mutant, GNL3 completely abolished DNA damage response induced by knockdown of endogenous GNL3. GNL3 interacts with the BLM-DNA2 helicase-nuclease complex and is critical for DNA end resection and subsequent RPA and RAD51 loading. The GNL3-BLM interaction requires SUMOylation and SUMO-interacting motifs (SIMs) of both proteins. We further showed that USP36, a nucleolar deubiquitinating enzyme, acts as a novel SUMO ligase for GNL3, whereas SUMOylated GNL3 can be deSUMOylated by the SUMO protease SENP3. Interestingly, several breast cancer-derived variants of GNL3 that interfere with its SUMOylation of SIM failed to interact with the BLM-DNA2 complex. Knockdown of GNL3 sensitizes breast cancer cells to the treatment with etoposide or Olaparib. Together, our results reveal that GNL3 SUMOylation is critical for HR repair and targeting GNL3 SUMOylation may induce HR deficiency and sensitize breast cancers to DNA damage-inducing agents.
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Project description:Androgen receptor (AR) signaling is a primary oncogenic driver of castration-resistant prostate cancer (CRPC), yet the mechanism remains incompletely understood. Through proteomic profiling of CRPC and primary PCa cells, we identify G Protein Nucleolar 3 (GNL3) as a novel AR coregulator. GNL3 physically interacts with AR, enhances its chromatin occupancy, and directly coactivates transcriptional programs that promote cell proliferation, including NEK2 and CDC20. Concurrently, GNL3 functions as a corepressor of immune-responsive genes such as CXCL10 and TAP1 via class I histone deacetylases (HDACs), thereby facilitating CD8+ T cell elimination and establishing an immunosuppressive tumor microenvironment. GNL3 expression and AR-GNL3 complex formation progressively increase from normal prostate to CRPC and correlate with poor clinical outcomes. Functionally, GNL3 knockdown sensitizes CRPC cells to AR antagonists and impairs tumor growth and metastasis. Furthermore, we demonstrate that combinatorial inhibition of NEK2, class I HDACs, and AR signaling can be a potential therapeutic strategy for CRPC. Overall, these findings establish GNL3 as a dual-function AR coregulator and therapeutic target, providing mechanistic insights into transcriptional regulation and immune evasion in advanced PCa.
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Project description:Androgen receptor (AR) signaling is a primary oncogenic driver of castration-resistant prostate cancer (CRPC), yet the mechanism remains incompletely understood. Through proteomic profiling of CRPC and primary PCa cells, we identify G Protein Nucleolar 3 (GNL3) as a novel AR coregulator. GNL3 physically interacts with AR, enhances its chromatin occupancy, and directly coactivates transcriptional programs that promote cell proliferation, including NEK2 and CDC20. Concurrently, GNL3 functions as a corepressor of immune-responsive genes such as CXCL10 and TAP1 via class I histone deacetylases (HDACs), thereby facilitating CD8+ T cell elimination and establishing an immunosuppressive tumor microenvironment. GNL3 expression and AR-GNL3 complex formation progressively increase from normal prostate to CRPC and correlate with poor clinical outcomes. Functionally, GNL3 knockdown sensitizes CRPC cells to AR antagonists and impairs tumor growth and metastasis. Furthermore, we demonstrate that combinatorial inhibition of NEK2, class I HDACs, and AR signaling can be a potential therapeutic strategy for CRPC. Overall, these findings establish GNL3 as a dual-function AR coregulator and therapeutic target, providing mechanistic insights into transcriptional regulation and immune evasion in advanced PCa.
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Project description:The regulation of replication forks stalling and replication origins firing must be tightly coordinated to prevents genomic instability. Here we show that GNL3/nucleostemin, a GTP-binding protein able to shuttle between the nucleolus and the nucleoplasm, limits replicative stress by limiting replication origins firing. GNL3 is in proximity of nascent DNA and its depletion reduces forks speed but increases forks density and replication origins firing. When subjected to exogenous replicative stress, cells impaired for GNL3 exhibits MRN-dependent resection and RPA phosphorylation. Strikingly, inhibition of origin firing using CDC7 inhibitor decreased resection in absence of GNL3 but not in absence of BRCA1, suggesting that GNL3 does not protect nascent strand directly from resection. Consistent with this, overexpression of GNL3 leads to an increased resection in response to replicative stress and enhanced origin firing efficiency. These data indicate that the probability of origins firing is tightly regulated by GNL3 to limit replicative stress. Finally, we show that ORC2 and GNL3 interacts together in the nucleolus. We propose a model where GNL3 level is crucial to determine the correct amount of ORC2 on chromatin by sequestrating it in the nucleolus thanks to the capacity of GNL3 to shuttle between nucleoplasm and nucleolus.
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