Notes

Components regarding Gasdermin Identification by simply Proteases.
r tissues to promote migration and invasion of breast cancer cells by up-regulating ARHGAP36 expression.
To explore the effect of dibenzyl trisulfide (DTS) on cell proliferation and apoptosis in human head and neck squamous cell carcinoma (HNSCC) HN30 cells.

The effects of DTS on proliferation of HNSCC cell lines HN30, HN12, and SCC25 were examined by assessing colony formation ability of the treated cells. The effect of different concentrations of DTS on viability of HN30 cells was assessed using MTT assay. HN30 cells were treated with 3, 10, or 30 μmol/L DTS for 24 h, and the cell apoptosis and mitochondrial membrane potential (MMP) were detected using flow cytometry with annexin Ⅴ-FITC/PI double staining and JC-1 fluorescent probe staining. Western blotting was performed to determine the protein expressions of caspase-3, cleaved caspase-3 and Bcl-2 in the treated cells. The phosphorylation levels of Akt and p53 in HN30 cells were detected using Western blotting after treatment with 10 μmol/L DTS for 0.5, 1, 2, 4, 8, or 16 h.

DTS at 1 μmol/L significantly inhibited the proliferation of HN30, HN12 and SCC25 cells as shown by colony formation assay. MTT assay showed that DTS dose-dependently decreased HN30 cell viability as compared with the solvent control group, and 100 μmol/L DTS produced the strongest inhibitory effect (
< 0.0001). Treatment with DTS below 30 μmol/L concentrationdependently promoted apoptosis (
< 0.01) and lowered the MMP (
< 0.01) of HN30 cells, and after treatment for 24 h, the cells showed significantly increased cleaved caspase-3 (
< 0.01) and decreased Bcl-2 expression (
< 0.01). Treatment with 10 μmol/L DTS for 16 h significantly inhibited Akt phosphorylation (
< 0.001) and enhanced p53 phosphorylation (
< 0.01) in HN30 cells.

DTS inhibits proliferation and induces apoptosis of HN30 cells possibly through mechanisms involving the inhibition of Akt and the activation of p53.
DTS inhibits proliferation and induces apoptosis of HN30 cells possibly through mechanisms involving the inhibition of Akt and the activation of p53.
To explore the role of fetuin B-AMPK/ACC signaling pathway in mediating the effect of puerarin on hepatic insulin resistance in mice with type 2 diabetes mellitus (T2DM).

Forty C57BL/6J mouse models of T2DM induced by high-fat diet and intraperitoneal injection of streptozotocin were randomized into diabetic model (HFD) group and 3 puerarin groups for treatment with low-, moderate- and high- dose puerarin (50, 100 and 200 mg/kg, respectively), with another 10 mice fed a normal diet as the control group. After treatment for 8 weeks, the mice were examined for fasting blood glucose (FBG), fasting insulin (FINS), liver triglycerides (TG), cholesterol (TC) and free fatty acids (FFA) levels. The expression of fetuin B in the liver was detected by immunohistochemistry. RT-qPCR was used to detect the expressions of fetuin B, AMPK, and ACC mRNA in the liver, and the protein expressions of fetuin B, AMPKα1, ACC, P-AMPKαT183/T172, and P-ACC S79 were determined with Western blotting.

Treatment with moderate- and high-dose puerarin significantly lowered TG, TC, FFA and FBG levels in diabetic mice (
< 0.01). Puerarin at all the 3 doses significantly lowered FINS and HOMA-IR of the mice (
< 0.01). selleck compound In diabetic mice, hepatic expressions of fetuin B and ACC mRNA increased and AMPK mRNA decreased significantly (
< 0.01); the protein expressions of fetuin B and ACC increased while those of AMPKα1, P-AMPKαT183/T172 and P-ACC S79 decreased significantly (
< 0.01). Puerarin dose-dependently inhibited the mRNA and protein expressions of fetuin B and ACC, increased AMPK mRNA and protein expressions of AMPKα1, P-AMPKαT183/ T172, and P-ACC S79, and lowered fetuin B content in the liver of diabetic mice (
< 0.01).

Puerarin alleviates insulin resistance and improves glucolipid metabolism in T2DM mice by modulating hepatic fetuin B-AMPK/ACC signaling pathway.
Puerarin alleviates insulin resistance and improves glucolipid metabolism in T2DM mice by modulating hepatic fetuin B-AMPK/ACC signaling pathway.
To investigate the expression of nicotinamide-N-methyltransferase (NNMT) in gastric cancer (GC) and explore its biological and clinicopathological significance.

We screened the candidate genes associated with the classification and prognosis of gastric cancer by analyzing GEO, Oncomine and TCGA datasets. The molecular pathways and protein interaction network involving these candidate genes were analyzed using STRING, GSEA, David and Cytoscape software. The expressions of the candidate genes in 28 pairs of gastric cancer and adjacent tissues were detected with qRTPCR, and CCK-8 assay, clone formation assay, wound healing assay and Transwell assay were carried out to analyze the effects of modulation of NNMT expression on proliferation, invasion and migration of different gastric cancer cell lines.

NNMT was highly expressed in gastric cancer tissues and was negatively correlated with the prognosis of patients with gastric cancer. Pathway analysis showed that the high expression of NNMT was associated withcells, suggesting the potential of NNMT as prognostic marker of gastric cancer.
NNMT is highly expressed in gastric cancer and negatively correlated with the prognosis of gastric cancer patients. The high expression of NNMT promotes the proliferation, invasion and metastasis of gastric cancer cells, suggesting the potential of NNMT as prognostic marker of gastric cancer.
To establish an efficient protocol for directed differentiation of miniature-swine induced pluripotent stem cells (iPSCs) into GABAergic progenitors in a chemically defined system.

We adopted a two-stage protocol for inducing the differentiation of porcine iPSCs. In the first stage, embryoid bodies (EBs) derived from porcine iPSCs after 3 days of suspension culture were induced in neural induction medium (containing SB431542, DMH1 and FGF2) till day 12 to differentiate into primitive neuroepithelia cells (NECs). In the second stage, the primitive NECs were induced in neural induction medium (containing Pur and B27) to obtain neural rosettes, which further differentiated into GABAergic neuron progenitors on day 21. After labeling with CM-DiI, the progenitor cells were stereotactically transplanted into the substantia nigra (SN) of 6-OHDA-lesioned PD model rats, and the cell survival, migration and differentiation in vivo were observed.

Porcine iPSCs could be passaged stably on the feeder cell layer and expressed the pluripotent stem cell markers OCT4, Nanog, SSEA1and TRA-160.
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