Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Identification of JMJD1C target genes in LN-229 glioblastoma cells.

ABSTRACT: JMJD1C shows ubiquitous expression and is often downregulated in tumor entities compared to healthy tissues.JMJD1C inhibit growth of the glioblastoma cell line LN-229. Here, JMJD1C knockdown leads to malignant progression in the glioblastoma cell line LN-229.

ORGANISM(S): Homo sapiens

PROVIDER: GSE166351 | GEO | 2021/02/09

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Identification of JMJD1C target genes in LN-229 glioblastoma cells.

Project description:Identification of JMJD1C target genes in LN-229 glioblastoma cells.

| PRJNA700586 | ENA

Effect of IDH1 mutation induced by doxycycline on gene expression during VSVΔ51 infection in LN-229-TRE-R132H glioblastoma cells

Project description:To investigate whether IDH1 mutation influence the effects of oncolytic virus VSVΔ51, we transduced doxycycline-inducible IDH1-R132H lentiviruses into LN-229 to establish the LN-229-TRE-R132H cell line. We then performed gene expression profiling analysis using data obtained from RNA-seq of LN-229-TRE-R132H cells infected with or without VSVΔ51 in the presence or absence of IDH1 mutation induced by doxycycline.

2023-09-19 | GSE208634 | GEO

RNA sequencing analysis of LN-229-shControl and LN-229-shMOB2 cells

Project description:RNA sequencing analysis of LN-229-shControl and LN-229-shMOB2 cells

| PRJNA579353 | ENA

Expression data from WIF1 induced LN-229 (GBM cell line)

Project description:Glioblastoma is the most aggressive primary brain tumor in adults and due to the invasive nature it cannot be completely removed. We have recently shown that the WNT inhibitory factor 1 (WIF1), a secreted inhibitor of WNTs, is downregulated in glioblastoma and acts as strong tumor suppressor. In search of a mediator for this function differential gene expression profiles of WIF1-expressing cells were performed. MALAT1, a long non-coding RNA and key positive regulator of invasion, emerged as the top downregulated gene. Indeed, knock-down of MALAT1 reduced migration in glioblastoma cells, without effect on proliferation. LN-229 cells induced with Doxocyclin to express WIF1 were compared to the non-induced control (two biological replicates each)

2015-02-23 | E-GEOD-58525 | biostudies-arrayexpress

Identification of LINC00152 target genes in comparison in A172 and U87 glioblastoma cells

Project description:The long noncoding RNA LINC00152 shows ubiquitous expression and is often upregulated in tumor entities compared to healthy tissues. LINC00152 promotes malignant progression in the glioblastoma cell line U87. Here, LINC00152 knockdown leads to a reduction of migration and invasion of tumor cells. However, LINC00152 seems to have an opposite effect in another glioblastoma cell line A172. For this reason, the transcriptional patterns after LINC00152 knockdown in both cell lines (U87 and A172) were compared to identify the differences.

2021-01-01 | GSE161352 | GEO

Jmjd1c

Project description:Jmjd1c

| PRJNA304620 | ENA

JMJD1C knockdown (H9_CT2_JMJD1C-KD_Microarray_JW)

Project description:It has been recently reported that the pluripotency factor OCT4, the early neural inducing factor NR2F2, and the pluripotency-associated miRNA miR-302 are linked in a regulatory circuitry that critically regulate both pluripotency and neural differentiation of human embryonic stem cells (hESCs). We show here that JMJD1C, a H3K9 demethylase expressed in undifferentiated hESCs, plays a key role in the regulatory circuitry. hESCs with JMJD1C knockdown (KD) retain the state of self-renewal and pluripotency, but express lower miR-302c than control hESCs. JMJD1C directly binds to the miR-302 promoter in hESCs and reduces H3K9 methylation on the promoter. Upon withdrawal of bFGF (an inhibitor of neural initiation) from a defined culture medium, the KD, but not control, hESCs differentiate into neural progenitors within three days – the fastest ever reported, accompanied by rapid increase of NR2F2 expression. A miR-302c analogue or an inhibitor of H3K9 methylation reduces neural induction from the KD hESCs, whereas a miR-302c inhibitor promotes hESC differentiation. Together, our findings suggest that JMJD1C plays a central role in control of neural differentiation from hESCs, which involves sustained miR-302c expression, and that inhibition of JMJD1C is sufficient to rapidly induce neural progenitors from hESCs in the defined medium depleted of bFGF. This is also the first evidence, to our knowledge, for epigenetic modification of miR-302 in hESCs. 6 human ES cell lines were used in this microarray assay. Each line has two replicates.

2013-12-24 | E-GEOD-46485 | biostudies-arrayexpress

shRNA Screening Identifies JMJD1C as being required for Leukemia Maintenance

Project description:We used a mouse model of human AML induced by the MLL-AF9 fusion oncogene, and an epigenetic shRNA library to screen for novel potential drug targets. One of the best candidate drug targets identified in these screens was Jmjd1c. Depletion of Jmjd1c impairs growth and colony formation of mouse MLL-AF9 cells in vitro, as well as establishment of leukemia after transplantation. Depletion of JMJD1C impairs expansion and colony formation of human leukemic cell lines, with the strongest effect observed in the MLL-rearranged ALL cell line, SEM. In both mouse and human leukemic cells, the growth defect upon JMJD1C depletion appears to be primarily due to increased apoptosis, which implicates JMJD1C as a potential therapeutic target in leukemia.

2013-08-22 | GSE50048 | GEO

shRNA Screening Identifies JMJD1C as being required for Leukemia Maintenance (Agilent)

2014-01-23 | E-GEOD-54311 | biostudies-arrayexpress

shRNA Screening Identifies JMJD1C as being required for Leukemia Maintenance (Agilent)

2014-01-23 | GSE54311 | GEO