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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Myrna Serrano

PROVIDER: E-GEOD-44601 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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.

2013-04-01 | GSE44601 | 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

SND1 is a novel regulator of endothelial function

Project description:Staphylococcal nuclease and tudor domain containing protein 1 (SND1), which is also known as p100 or Tudor-SN, is a recently identified protein that is highly expressed in multiple cancers including breast cancer, liver cancer, and colon cancer. Endothelial function and vascular integrity are critical modulators in cancer metastasis and progression. Although much progress has been made in studying SND1’s oncogenic role, the involvement of SND1 in endothelial function has never been explored.

2024-10-30 | GSE219194 | GEO

SND1-SMARCA5 interaction strengthened by PIM promoted the proliferation, metastasis and chemoresistance of ESCC

Project description:Chromatin remodeling plays a pivotal role in the progression of esophageal squamous cell carcinoma (ESCC), yet the precise mechanisms remain poorly understood. Here, we elucidate the critical function of staphylococcal nuclease and tudor domain-containing 1 (SND1) in modulating chromatin dynamics, thereby driving ESCC progression in both in vitro and in vivo models. Our data revealed that SND1 was markedly overexpressed in ESCC cell lines. Silencing SND1 disrupted histone modifications, attenuated RNA polymerase II activity, and precipitated increased chromosomal aberrations and DNA damage, particularly following camptothecin treatment. These molecular perturbations culminated in diminished cellular proliferation, metastasis and chemoresistance. We further identified that the regulatory effects of SND1 on chromatin are mediated through its interaction with SMARCA5, a process potentiated by PIM1-catalyzed phosphorylation of SND1 at serine 426. This SND1-SMARCA5 interaction is essential for the transcriptional activation of CUX1, a key oncogene implicated in ESCC progression. Notably, disruption of SND1S426 phosphorylation impaired the SND1-SMARCA5 interaction, leading to significant inhibition of ESCC tumor growth and metastatic potential in vivo. Our findings unveil a novel mechanistic axis involving SND1 and SMARCA5 in chromatin remodeling and oncogenesis, offering promising therapeutic targets for ESCC intervention.

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Project description:Danio rerio snd1, staphylococcal nuclease and tudor domain containing 1 [Source:NCBI gene;Acc:324404], is expressed in 1 baseline experiment(s);

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