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Gene expression data from HepG2 SND1 knockdown stable cell lines after 5-Fu treatment

ABSTRACT: Gene expression data from HepG2 SND1 knockdown stable cell lines after 5-Fu treatment

PROVIDER: PRJNA471413 | ENA |

REPOSITORIES: ENA

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Gene expression data from HepG2 SND1 knockdown stable cell lines after 5-Fu treatment

Project description:Gene expression data from HepG2 SND1 knockdown stable cell lines after 5-Fu treatment

| PRJNA471413 | ENA

Gene expression data from HepG2 SND1 knockdown stable cell lines after 5-Fu treatment

Project description:SND1 protein is a highly conserved protein of eukaryotic cells and is involved in a group of cellular biological processes, such as gene transcription, pre-mRNA splicing, cell cycle, DNA damage repair, proliferation and programmed cell death degradome, adipogenesis and cancerogenesis. SND1 can promote the metastasis and proliferation of breast cancer cells by down-regulating the miR-127 expression. Herein, we used microarrays to detail the potential molecular mechanism in the chemotherapy drug-induced HCC apoptosis.

2018-12-26 | GSE114447 | GEO

Genome map of SND1 binding sites by ChIP-chip analysis in human HepG2 cells under inflammatory conditions.

Project description:Profiling of promoter occupancy by SND1 coactivator in human hepatoma cells. Control and TNFα-treated HepG2 cells are immunoprecipitated with anti-SND1 antibody and input and immunoprecipitated material were hybridized in an Agilent human promoter microarray Two-condition experiment. Biological replicates: 3 control replicates, 3 TNFα-treated replicates. Input vs. Immunoprecipitated material

2015-07-31 | E-GEOD-61539 | biostudies-arrayexpress

Expression data from SND1 knockdown clones of human HCC cell line QGY-7703

Project description:Staphylococcal nuclease domain-containing protein 1 (SND1) is overexpressed in human hepatocellular carcinoma (HCC) and positively regulates development and progression of HCC. We established stable clones expressing SND1 shRNA in QGY-7703 cells and analyzed the gene expression profiles of a control clone and two SND1 knockdown clones to check what genes are regulated by SND1. Steady-state proliferating cells were collected for RNA extraction and Affymetrix microarray hybridization. Three biological replicates each of a control clone and 2 SND1 knockdown clones.

2013-04-01 | E-GEOD-44601 | biostudies-arrayexpress

Expression data from SND1 knockdown clones of human HCC cell line QGY-7703

2013-04-01 | GSE44601 | GEO

Genome map of SND1 binding sites by ChIP-chip analysis in human HepG2 cells under inflammatory conditions.

2015-07-31 | GSE61539 | GEO

Gene expression data from SKOV3 cell line with SND1 knockdown

2021-06-13 | GSE115784 | GEO

HepG2 TP53BP2-knockdown

Project description:HepG2 TP53BP2-knockdown

| PRJNA854656 | ENA

shRNA RNA-seq from HepG2 (ENCSR398LZW)

Project description:shRNA knockdown against SND1 in HepG2 cells followed by RNA-seq. (SND1 BGHLV14) For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf

2016-05-26 | GSE80884 | GEO

The methylarginine reader function of SND1 is oncogenic

Project description:Staphylococcal nuclease Tudor domain containing 1 (SND1) protein is an oncogene that “reads” methylarginine marks through its Tudor domain. Specifically, it recognizes methylation marks deposited by protein arginine methyltransferase 5 (PRMT5), which is also known to promote tumorigenesis. SND1 is a known driver of hepatocellular carcinoma, but it is unknown if the Tudor domain is needed to drive this disease. We sought to identify the biological role of the SND1 Tudor domain in normal and tumorigenic settings. To do so, we developed two genetically engineered SND1 mouse models, namely a knockout (Snd1 KO) and a Snd1 Tudor domain mutated (Snd1 KI) mouse. Transcriptome analysis of normal KO and KI liver samples reveals a role for the SND1 Tudor domain in regulating expression of major acute phase proteins (APPs) and genes involved in the unfolded protein response (UPR), which could provide mechanistic insight into SND1’s functions in a tumor setting. These processes may provide insight into how SND1 functions as an oncogene. These results support the use of PRMT5 inhibitors, and the development of small molecule inhibitors that target the SND1 Tudor domain, as novel treatments for HCC.

2024-09-07 | GSE237559 | GEO

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