Publication | Open Access
Too much heparin: possible source of error in blood gas analysis.
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Citations
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References
1983
Year
ApoptosisImmunologyPathologyCell DeathMuch HeparinCancer BiologySoluble TrailTumor BiologyMetastatic Hepatoma CellsHematologyTumor ImmunityCancer Cell BiologyClinical ChemistryLaboratory MedicineCancer ResearchHeparinsHealth SciencesLiver PhysiologyCell BiologyDeath Receptors Dr4Possible SourceCancer ImmunosurveillanceBlood Gas AnalysisHemostasisCoagulopathyMedicineBlood Transfusion
Metastatic hepatoma cells are the most dangerous parts in hepatocarcinoma patients.We want to study the mechanism of metastatic hepatoma cells to escaping from host immune attacks. Firstly, we constructed the metastatic hepatoma cell model by using plates pre-coated with Poly-HEMA and found that they were aggregated, proliferation-resistant, apoptosis-resistant, cell cycle arrested and more invasive. These metastatic hepatoma cells could settled down and proliferated again under suitable conditions. Subsequently,we investigated the response of metastatic hepatoma cells to the typical immune surveillant molecule TNF-related apoptosis-inducing ligand (TRAIL). The data indicated that metastatic hepatoma cells not only resist to TRAIL-induced apoptosis, but also express lower membrane binding TRAIL and excrete more soluble TRAIL (sTRAIL) to exert a stealth "tumor counterattack" effect to attack immune effector cells. Deeply study found that the membrane binding death receptors DR4 and DR5 were down-regulated on metastatic BEL7402 and SMMC7721 cells and that their active level of caspase-8,-9,-3 was highly restrained. So we concluded that metastatic hepatoma cells could escape from host immune system by the death receptor pathway. This work was supported by grants from the National Natural Science Foundation of China (No.30873025, No.30700357 and No.30772031), Corresponding author E-mail:WSW@sdu.edu.cn.
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