Transcriptomic analysis of RCH-ACV cells whose SETDB2 was knocked down by shRNA
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PROVIDER: PRJNA515882 | ENA |
REPOSITORIES: ENA
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Project description:RCH-ACV cells was depleted for SETDB2 by shRNA lentivirus construct co-expressing mCherry fluorescent. After sorting of mCherry positive cells, the cells were cultured and expanded and total RNA was extracted for Microarray experiment.
2019-01-19 | GSE125329 | GEO
Project description:As the primary driving forces of gastrulation, convergence and extension (C&E) movements lead to a medio-lateral narrowing and an anterior-posterior elongation of the embryonic body axis. Histone methylation as a post-translational modification plays a critical role for early embryonic development, but its functions on C&E movements remaine largely unknown. Here, we uncover that knockdown of setdb2, a SET domain-containing protein possessing potential histone H3K9 methyltransferase activity, induces abnormal C&E movements. Then, we perform genome-wide gene expression profiling of zebrafish in 6h control embryos and setdb2 morphant embryos to address the downstream target of setdb2 gene.
2014-06-20 | E-MTAB-2207 | biostudies-arrayexpress
Project description:Histone H3 lysine 9 tri-methyltransferases (H3K9me3) are related to transcriptional gene silencing. Although SETDB2 has H3K9me3 activity, it is unknown whether SETDB2 is linking to carcinogenesis. Here, we studied alterations and functions of SETDB2 in gastric cancers (GCs). In human clinical samples, overexpression of SETDB2 protein was observed in 30 of 72 (41.7%) primary GC tissues compared with their normal counterparts, and significantly associated with poor prognosis of the patients (P<0.05). SETDB2 protein was significantly detected in late stage of GCs. Moreover, SETDB2 protein was strongly expressed in four (30.8%) of 13 GC cell lines, and knockdown of SETDB2 led to decrease the cell proliferation, migration and invasion. According to the microarray analysis on a GC cell line after knockdown of SETDB2, the expression of WWOX and CADM1 tumor suppressor genes was significantly up-regulated. ChIP analysis showed that the H3K9me3 levels at the promoter regions of WWOX and CADM1 genes were closely regulated by the SETDB2 in GC cells. We also found that SETDB2 bound to the promoter regions after SETDB2 overexpression. Our data suggest that SETDB2 is associated with transcriptional repression of WWOX and CADM1, through H3K9me3, and hence overexpression of SETDB2 may contribute to gastric progression. Transfection of SETDB2 siRNA into MKN74 cells were performed by electroporation. After 48hrs, cells were harvested. Total RNA was used for cDNA microarray.
2016-02-21 | E-GEOD-76135 | biostudies-arrayexpress
Project description:Histone H3 lysine 9 tri-methyltransferases (H3K9me3) are related to transcriptional gene silencing. Although SETDB2 has H3K9me3 activity, it is unknown whether SETDB2 is linking to carcinogenesis. Here, we studied alterations and functions of SETDB2 in gastric cancers (GCs). In human clinical samples, overexpression of SETDB2 protein was observed in 30 of 72 (41.7%) primary GC tissues compared with their normal counterparts, and significantly associated with poor prognosis of the patients (P<0.05). SETDB2 protein was significantly detected in late stage of GCs. Moreover, SETDB2 protein was strongly expressed in four (30.8%) of 13 GC cell lines, and knockdown of SETDB2 led to decrease the cell proliferation, migration and invasion. According to the microarray analysis on a GC cell line after knockdown of SETDB2, the expression of WWOX and CADM1 tumor suppressor genes was significantly up-regulated. ChIP analysis showed that the H3K9me3 levels at the promoter regions of WWOX and CADM1 genes were closely regulated by the SETDB2 in GC cells. We also found that SETDB2 bound to the promoter regions after SETDB2 overexpression. Our data suggest that SETDB2 is associated with transcriptional repression of WWOX and CADM1, through H3K9me3, and hence overexpression of SETDB2 may contribute to gastric progression.
2016-02-21 | GSE76135 | GEO
Project description:The persistent headaches characteristic of chronic migraine may stem from the activation and sensitization of primary afferent neurons within the trigeminovascular pathway. The molecular basis for this pathophysiology, however, remains incompletely understood. In this study, we demonstrated that SETDB2, a histone methyltransferase expressed in trigeminal ganglion (TG) neurons, plays a pivotal role in facilitating migraine-associated pain behaviors. We modelled chronic headache with repeated administration of nitroglycerin (NTG, a well-recognized migraine trigger in migraineurs) and observed a notable upregulation of SETDB2 in mouse TG neurons following NTG treatment. A comparable increase was also identified in the cerebrospinal fluid of migraine sufferers. Reversing the NTG-induced SETDB2 upregulation abrogated the increased trimethylation of histone H3K9 (H3K9me3) and alleviated established migraine-associated pain behaviors. Conversely, mimicking the upregulation of SETDB2 in intact TG neurons was sufficient to induce pain hypersensitivity. Moreover, we found that SETDB2 upregulation induced by NTG prevented the binding of the transcription factor KLF4 to the promoter of the insulin-degrading enzyme (Ide) gene. This, in turn, inhibited IDE expression, and hindered the degradation of calcitonin- gene-related peptide (CGRP), a promising target for preventing migraine, in TG neurons. Targeting the sensory SETDB2-KLF4-IDE transcriptional axis may present novel therapeutic opportunities for treating migraine.
2026-02-28 | GSE308024 | GEO
Project description:Macrophage transition from an inflammatory to reparative phenotype after tissue injury is controlled by epigenetic enzymes that regulate inflammatory gene expression. We have previously identified the histone methyltransferase, SETDB2, in macrophages drives tissue repair by repressing NFκB-mediated inflammation. Complementary ATAC and RNA sequencing of wound macrophages isolated from mice deficient in SETDB2 in myeloid cells revealed that SETDB2 suppresses the inflammatory gene program by inhibiting chromatin accessibility at NFkB-dependent gene promoters. We found that STAT3 was required for SETDB2 expression in macrophages yet, paradoxically, it also functioned as a binding partner of SETDB2 where it repressed SETDB2 activity by inhibiting its interaction with the NFKB component, RELA, leading to increased RELA/NFKB-mediated inflammatory gene expression. Further, RNA sequencing in wound macrophages from STAT3-deficient mice corroborated this and revealed STAT3 and SETDB2 transcriptionally co-regulate overlapping genes. Finally, in diabetic wound macrophages STAT3 expression and STAT3-SETDB2 binding were increased. As such, we identify what we believe to be a novel SETDB2-STAT3 axis that modulates macrophage phenotype during tissue repair and may be an important therapeutic target for nonhealing diabetic wounds.
2024-11-06 | GSE274112 | GEO
Project description:Objective: This study aimed to investigate SETDB2 expression, clinical significance, and molecular mechanism in thyroid cancer progression. Methods: SETDB2 expression and prognosis were analyzed using TCGA and CPTAC databases, and validated by immunohistochemistry in 90 clinical samples (primary, recurrent, metastatic papillary, and anaplastic carcinoma). Overexpression and knockdown models were established in BCPAP and BHT101 cells. Proliferation was assessed by CCK‑8, colony formation, and EdU assays. RNA‑seq and qPCR identified downstream targets, with rescue experiments via U2AF1 overexpression. Results: SETDB2 was significantly downregulated in recurrent and metastatic papillary and anaplastic thyroid carcinoma, and low expression correlated with poor prognosis. SETDB2 overexpression suppressed proliferation and colony formation in anaplastic BHT101 cells, whereas knockdown promoted growth in papillary BCPAP cells. U2AF1 was identified as a key downstream target, and its overexpression partially reversed the inhibitory effects of SETDB2 on proliferation. Conclusion: SETDB2 acts as a tumor suppressor in thyroid cancer; its loss promotes progression, likely through regulating U2AF1. The SETDB2‑U2AF1 axis represents a potential therapeutic target.
2026-08-11 | GSE342848 | GEO
Project description:Podocyte dysfunction represents both an early pathological hallmark and a key driver of proteinuria in diabetic kidney disease (DKD); however, the epigenetic mechanisms underlying this process remains poorly defined. Here, we identify the histone methyltransferase SETDB2 as a pivotal epigenetic suppressor of podocyte dysfunction and DKD progression. Glomerular SETDB2 expression is markedly reduced in both DKD patients and mouse models, showing an inverse correlation with disease severity. Podocyte-specific SETDB2 deficiency exacerbates podocytes dysfunction and accelerates DKD progression, whereas its overexpression exerts renal protective effects. Mechanistically, SETDB2 directly enhances H3K9 trimethylation at the Smad3 promoter, thereby repressing SMAD3 expression and activation, ultimately preserving podocyte function. Notably, we identify TCF21, a transcription factor downregulated in DKD, as a direct upstream regulator of Setdb2 expression via promoter binding and transcriptional activation. Collectively, these findings establish SETDB2 as a key regulator of podocyte integrity and a promising therapeutic target for DKD.
2026-07-31 | GSE303915 | GEO
Project description:Pseudobutyrivibrio sp. ACV-2 Genome sequencing
| PRJNA254888 | ENA
Project description:RNA-seq data of NKX6-3 knockdown in the BCP-ALL cell line RCH-ACV
| PRJEB92217 | ENA