Gene expression profiles and protein-protein interaction networks in neuroblastoma with MEIS2 depletion.

Purpose: The purpose of the present study was to identify differential gene expressions (DEGs) and key pathways in neuroblastoma with MEIS2 depletion through bioinformatics.

Methods: The microarray gene expression dataset GSE56003 was downloaded from the Gene Expression Omnibus (GEO) database. DEGs were identified using Gene Level RMA sketch and Transcriptome Analysis Console.

Piracetam ameliorated oxygen and glucose deprivation-induced injury in rat cortical neurons via inhibition of oxidative stress, excitatory amino acids release and P53/Bax.

Our previous work has demonstrated that piracetam inhibited the decrease in amino acid content induced by chronic hypoperfusion, ameliorated the dysfunction of learning and memory in a hypoperfusion rat model, down-regulated P53, and BAX protein, facilitated the synaptic plasticity, and may be helpful in the treatment of vascular dementia. To explore the precise mechanism, the present study further evaluated effects of piracetam on Oxygen and glucose deprivation (OGD)-induced neuronal damage in rat primary cortical cells. The addition of piracetam to the cultured cells 12 h before OGD for 4 h significantly reduced neuronal damage as determined by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay and lactate dehydrogenase release experiments.

[The advantages for Snail expression to promote cell migration and induce actin reorganization and to protect against the serum-deprivation-triggered apoptosis of bone marrow stem cells].

The Snail transcription factor has been described as a strong repressor of E-cadherin and its stable expression induces epithelial-mesenchymal transitions responsible for the acquisition of motile and invasive properties during tumor progression. A fascinating analogy that has been raised is the seemingly similar and shared characteristics of stem cells and tumorigenic cells, which prompted us to investigate whether the mechanisms of the acquisition of invasiveness during tumor progression are also involved in bone marrow stem cells (MSCs). In this study, we examined whether Snail gene expression acts in the mobility, cytoskeleton and anti-apoptosis of MSCs.

Zinc-finger transcription factor snail accelerates survival, migration and expression of matrix metalloproteinase-2 in human bone mesenchymal stem cells.

Although bone mesenchymal stem cells (BMSC) hold promise in gene therapy and tissue engineering, the inefficient migration and the low capability of subsequent survival of BMSC have largely restrained progress in these studies. Characteristics shared between stem cells and tumorigenic cells prompted us to investigate whether mechanisms of tumor progression contribute to stem cell migration. The transcription factor Snail which functions in epithelial-mesenchymal transitions (EMT) is responsible for the acquisition of motile and invasive properties of tumor cells.

[Expression of Snail and E-cadherin in pancreatic carcinoma and clinical significance thereof].

Objective: To investigate the expression of Snail, a newly discovered inhibitory transcription factor, and E-cadherin in pancreatic carcinoma (PC) and clinical significance thereof.

Methods: Immunohistochemistry was used to examine the expression of Snail and E-cadherin in 56 specimens of PC obtained during operation. PC cells of the line of Panc-1 and transfected with pCMV-Tag2B-Snail, a eucaryotic expression vector coding Snail, so as to obtain a stable clone named Panc-1-Snail.