RNA Sequencing of L1-FGGY- and L1-FGGY+ lung squamous cell carcinoma tissues
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE181043 | GEO | 2022/07/27
REPOSITORIES: GEO
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Project description:In order to explore pathways which were affected by L1-FGGY in lung squamous cell carcinoma (LUSC), we performed RNA sequencing on L1-FGGY+/- LUSC tumor samples. We identified 1529 (826 up and 703 down) dysregulated genes in L1-FGGY positive tissues with an adjusted p value less than 0.05. The KEGG enrichment analysis indicated that many signaling pathways were upregulated in L1-FGGY positive tissues, including glutathione metabolism, metabolism of xenobiotics by cytochrome P450, arachidonic acid metabolism, metabolic pathways, and glycerolipid metabolism, most of which were metabolic pathways, especially in lipid-related metabolism.
2019-01-04 | GSE124625 | GEO
Project description:Mobile elements are important evolutionary forces that challenge genomic integrity. Long interspersed element-1 (L1, also known as LINE-1) is the only autonomous transposon still active in the human genome. It displays an unusual pattern of evolution, with at any given time a single active L1 lineage amplifying to thousands of copies before getting replaced by a new lineage likely under pressure of host restriction factors, which act notably by silencing L1 expression during early embryogenesis. Here, we demonstrate that in human embryonic stem cells (hESC) KAP1, the master co-factor of KRAB-containing zinc finger proteins (KRAB-ZFP) previously implicated in the restriction of endogenous retroviruses, represses a discrete subset of L1 lineages predicted to have entered the ancestral genome between 26.8 and 7.6 million years ago. In the mouse, we documented a similar chronologically conditioned pattern, albeit with a much contracted time scale. We could further identify an L1-binding KRAB-ZFP, suggesting that this rapidly evolving protein family is more globally responsible for L1 recognition. KAP1 knockdown in hESC induced the expression of KAP1-bound L1 elements, but their younger, human-specific counterparts (L1Hs) were unaffected. Instead, they were stimulated by depleting DNA methyltransferases, consistent with recent evidence demonstrating that the PIWI-piRNA pathway regulates L1Hs in hESC. Altogether, these data indicate that the early embryonic control of L1 is an evolutionary dynamic process, and support a model whereby newly emerged lineages are first suppressed by DNA methylation-inducing small RNA-based mechanisms, before KAP1-recruiting protein repressors are selected. HA-tagged Gm6871 ChIP-seq in mES cells, RNA-seq in control and Gm6871 KD mES cells, KAP1 ChIP-seq in WT mES cells, RNA-seq in control and DNMTs KD hES cells.
2014-06-09 | E-GEOD-58323 | biostudies-arrayexpress
Project description:Long interspersed elements-1 (LINE-1, L1) are retrotransposons that hold the capacity of selfpropagation in the genome with potential mutagenic outcomes. How somatic cells restrict L1 activity and how this process becomes dysfunctional during aging and in cancer cells is poorly understood. L1s are enriched at lamin associated domains, heterochromatic regions of the nuclear periphery. Whether this association is necessary for their repression has been elusive. Here we show that the sirtuin family member SIRT7 participates in the epigenetic transcriptional repression of L1 genome-wide in both mouse and human cells. SIRT7 depletion leads to increased L1 expression and retrotransposition. Mechanistically, we identify a novel interplay between SIRT7 and Lamin A/C in L1 repression. Our results demonstrate that SIRT7-mediated H3K18 deacetylation regulates L1 expression by promoting L1 association with elements of the nuclear lamina. The failure of such activity might contribute to the observed genome instability and compromised viability in SIRT7 knockout mice. Overall, our results reveal a novel function of SIRT7 on chromatin organization by mediating the anchoring of L1 to the nuclear envelope, and a new mechanism by which the nuclear lamina maintains genome integrity.
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2016-10-07 | PXD003696 | Pride
Project description:Mobile elements are important evolutionary forces that challenge genomic integrity. Long interspersed element-1 (L1, also known as LINE-1) is the only autonomous transposon still active in the human genome. It displays an unusual pattern of evolution, with at any given time a single active L1 lineage amplifying to thousands of copies before getting replaced by a new lineage likely under pressure of host restriction factors, which act notably by silencing L1 expression during early embryogenesis. Here, we demonstrate that in human embryonic stem cells (hESC) KAP1, the master co-factor of KRAB-containing zinc finger proteins (KRAB-ZFP) previously implicated in the restriction of endogenous retroviruses, represses a discrete subset of L1 lineages predicted to have entered the ancestral genome between 26.8 and 7.6 million years ago. In the mouse, we documented a similar chronologically conditioned pattern, albeit with a much contracted time scale. We could further identify an L1-binding KRAB-ZFP, suggesting that this rapidly evolving protein family is more globally responsible for L1 recognition. KAP1 knockdown in hESC induced the expression of KAP1-bound L1 elements, but their younger, human-specific counterparts (L1Hs) were unaffected. Instead, they were stimulated by depleting DNA methyltransferases, consistent with recent evidence demonstrating that the PIWI-piRNA pathway regulates L1Hs in hESC. Altogether, these data indicate that the early embryonic control of L1 is an evolutionary dynamic process, and support a model whereby newly emerged lineages are first suppressed by DNA methylation-inducing small RNA-based mechanisms, before KAP1-recruiting protein repressors are selected.
2014-06-09 | GSE58323 | GEO
Project description:We postulated that the primary DNA sequences, particularly abundant repetitive elements embedded in the genome, may instruct genome folding. Short and long interspersed nuclear elements (SINEs and LINEs, respectively) are two predominant sub-families of retrotransposons in most mammals. LINE-1 (LINE1 or L1) constitutes the most abundant type of repeat subclasses, making up to 18.8% and 17% (0.9~1.0 million copies) of the genome in mouse and human, respectively. B1 in mouse and its closely related, primate-specific Alu elements in human are the most abundant subclass of SINEs, constituting 2.7%~10% (0.6~1.4 million copies) of mouse and human genomes. Here, we demonstrate that B1/Alu and L1 repeats demarcate the genome into the A/B compartments and serve as the blueprint for the three-dimensional (3D) organization of mammalian genomes. Our finding explains the robustness and evolutionary conservation of nuclear chromatin organization in mammals. H3K9me3 ChIP-seq upon L1 AMO treatment; We electrotransfected L1 AMO into mESC to block L1 transcripts for 36 h and a standard control from GenTools was used as control -"SCR". We performed H3K9me3 ChIP-seq in mESCs treated with L1 or SCR AMO for 36 h. We found that L1 AMO did not alter the genome-wide binding of H3K9me3, ruling out the possibility that the loss of organization relates to changes in local heterochromatin marks.
2020-12-04 | GSE123806 | GEO
Project description:Although membrane-anchored Pd-l1 has been well-studied for its engagement with PD-1 on T cells to evade anti-tumor immunity, whether Pd-l1 regulate oncogenic signaling pathways in tumor cells remains elusive. In this experiment, to further dissect roles of the K262 residue acetylation for Pd-l1 nuclear function, we profiled RNA expression of WT or K262Q mutant mouse Pd-l1 re-expressed in CT26 KO Pd-l1 cells. Methods: Total RNA fromCT26/Vector, CT26/WT or CT26 Pd-l1 KO cells was purified using Qiagen RNeasy mini kit (Qiagen) according to the manufacturer’s instructions. Library preparation and sequenceing analysis were performed by BGI-Hong Kong Co. Ltd. Conclusions: Our study indicates that Pd-l1 acetylation modification may affect its function in nuclear.
2020-06-07 | GSE146557 | GEO
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