ABSTRACT
The LIM domains proteins are of significance proteins of human tumors. LMO3, a member of LIM-only subclass of LIM proteins, participates in the occurrence and development in many kinds of tumors, including neuroblastoma, meningioma, lung cancer and hepatocellular carcinoma, etc. LMO3 functions as interacting with neuronal transcription factor, HUA enhancer 2, interacting with upstream gene and inhibits its transcriptional activity or directly interacting with gene signaling. As an incomparable role in processes of tumors, LMO3 contributes to huge opportunities for therapeutic targeting for the future of the field.This article focuses on the molecular mechanism of LMO3 in the process of tumor development and metastasis, and reviews its recent progress.
ABSTRACT
The LIM domains proteins are of significance proteins of human tumors.LMO3,a member of LIM-only subclass of LIM proteins,participates in the occurrence and development in many kinds of tumors,including neuroblastoma,meningioma,lung cancer and hepatocellular carcinoma,etc.LMO3 functions as interacting with neuronal transcription factor,HUA enhancer 2,interacting with upstream gene and inhibits its transcriptional activity or directly interacting with gene signaling.As an incomparable role in processes of tumors,LMO3 contributes to huge opportunities for therapeutic targeting for the future of the field.This article focuses on the molecular mechanism of LMO3 in the process of tumor development and metastasis,and reviews its recent progress.
ABSTRACT
Aerobic glycolysis,which is also termed as Warburg effect,is one of the most common and profound biochemical phenotypes of tumor ceils.Several oncogenes and tumor suppressors genes have been implicated in aerobic glycolysis.MicroRNAs can control this metabolic switch by regulating oncogenes and tumor suppressors genes in a post-transcriptional way.A deeper understanding of the mechanisms and pathways by which miRNAs regulate the aerobic glycolysis will hopefully lead to a new therapeutic strategy for malignant cancer.
ABSTRACT
Liquid therapy is a vital method of perioperative treatment.Choosing correct kinds of transfusion and reasonable therapy strategies can significantly reduce the perioperative complications and shorten days in hospital and improve the critical patients prognosis.The historical development of perioperative liquid therapy is a forward process,which is about crystalloids vs.cilloid,dry vs.wet,and other controversial problems continuing to be summarized,explored and discussed.In this process,there are some specific perioperative treatment strategies with the physician having a deeper cognitive,such as goal-directed therapy,early goal directed therapy and fast track surgery which have significant clinical curative effect.This article summarizes the advance of perioperative liquid therapy.
ABSTRACT
Objective To observe the effect of combined treatment with rhTRAIL(recombinant human TNF-related apoptosis inducing ligand) and selective Cox-2 inhibitor Celecoxib on gallbladder carcinoma in vitro and to explore the possible mechanism of the effect. Methods Western blot analysis was used to detect the expression of c-FLIP and death receptors after treatment by Celecoxib. Apoptosis of gallbladder cell line SGC-996 after the combined treatment with Celecoxib and rhTRAIL was detected in three ways: (1) phase microscopy of the cells, (2) detection of effector caspase-3 and caspase-7 activity, and (3) determination of the proportion of apoptotic cells labeled by Annexin V-PI flow cytometric analysis using CELLQUEST software. Results Celecoxib down-regulated the expression of c-FLIPs and up-regulated the expression of DR5 in a dose- and time-dependent mode on cell line SGC-996. Apoptotic levels in the combined treatment group in cell line SGC-996 were significantly higher than those in the single drug treatment group and control group. Conclusion Celecoxib markedly sensitized rhTRAIL-induced apoptosis through the down-regulation of c-FLIPs and up-regulation of DR5 in gallbladder carcinoma cell line SGC-996.
ABSTRACT
MicroRNA(miRNA) is a kind of small non-coding RNA which contents 18-25 nucleotide (nt). MiRNA plays an important role in human tumor of digestive system. Recently lots of research demonstrates that miRNA can act either as oncogenes or as tumor suppressor genes or sometimes as both. And many families of miRNAs'targets have been found. So the study of miRNA will supply a new way to the diagnosis and therapy of digestive diseases.
ABSTRACT
Objective To explore the protective effect of treatment of somatostatin combined with growth hormone on brain injury in early severe acute pancreatitis(SAP)rats, and to investigate the relationship between brain injury and ratio of endothelin 1(ET 1) /nitric oxide(NO). Methods SAP model was established by retrograde pancreatic bile duct injection of 3.5% sodium taurocholate at a dose of 2.5 ml/kg in rats. Eighty SAP rats were equally divided into SAP group, somatostatin (S) group (introvenous injection of somatostatin at a dose of 42 ?g/kg once a day for 2 days), somatotropin (G) group (subcutaneous injection of somatotropin at a dose of 0.5 ?g/kg once a day for 2 days) and S+G group. Twenty normal rats were used as controls. The changes of encephaledema and blood brain barrier permeability were measured by dry wet method and Evan′s blue staining, respectively. Apoptosis of brain cells was detected by TUNEL method, and the ratio of serum ET 1/NO was also determined. Results The ratio of serum ET 1/NO was remarkably increased in SAP rats, which was correlated with the intensity of brain edema, permeability of blood brain barrier and apoptosis of brain cells. The treatment of somatostatin combined with growth hormone reduced the ratio of ET 1/NO and thus decreased the intensity of encephaledema, the permeability of blood brain barrier and apoptosis of brain cells. The changes of the brain slow wave were found simultaneously by electroencephalography in SAP rats after the therapy. Conclusions The treatment of somatostatin combined with growth hormone in SAP rats can inhibit serum ET 1/NO, prevent the development of brain edema, decrease the permeability of blood brain barrier, and alleviate the brain cells apoptosis. All these result in the relief of the brain injury.