ABSTRACT
Aim Toinvestigatewhetherexposureto Sanguinarine (SAN ) can inhibit cell proliferation in human mammary adenocarcinoma cells (MCF-7 ) and thepossiblemechanism.Methods WeexposedMCF-7 to anticancer compound SAN,cell viability was as-sessed by using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT ) reduction assay. ROS was measured using confocal microscopy,expres-sion of caspase-3 ,caspase-8 and caspase-9 were calcu-latedusingchemiluminescencemethod.Results SAN remarkably inhibited growth of human mammary adeno-carcinoma MCF-7 cells by decreasing cell proliferation. ROS release and caspase-3,caspase-8,caspase-9 ex-pression were stimulated by SAN in MCF-7 ,and these changes were abolished by the antioxidant,N-acetyl-cysteine(NAC).Conclusion Regulationofcaspases expression and release from MCF-7 cells are possibly e-voked by SAN through reactive oxygen species.
ABSTRACT
Recent studies have showed that RNAs regulate each other with microRNA ( miRNA ) response elements ( MREs ) , and this mechanism is known as “competing endogenous RNA (ceRNA)” hypothesis. Long noncoding RNAs(lncRNAs) are non-protein coding transcripts longer than 200 nucleotides. Ab-errant expression of lncRNAs has been found associated with gastric cancer, one of the most malignant tumors. Compelling evidence suggests that lncRNAs can interact with miRNAs and regulate the expression of miRNAs as ceRNAs. Several lncRNAs such as GAPLINC, BC032469, H19, HOTAIR, FER1L4 and MEG3 have been found to be associated with miRNAs in gastric cancer( GC) . It is tempting to speculate that a multitude of ln-cRNAs may interrupt definitive steps in GC suppressive and on-cogenic pathways. The uncovering of the underlying mechanisms of lncRNAs may benefit our understanding of gastric cancer′s pathogenesis.
ABSTRACT
It has been confirmed that genetic factor plays an im-portant role in the pathogenesis of depression. MTHFR is one of the key enzymes in folate and homocysteine ( Hcy ) metabolism which participates in Alzheimer’ s disease, depression and other mental illnesses. MTHFR-677C/T polymorphism causes the de-crease of enzyme activity and heat resistance, which will lead to lower folate and elevated plasmal Hcy concentration. All of these results put together will cause the central neuronal damage and microvascular damage and affect the synthesis of central neuro-transmitter and methylation of biogenic amines and phospholipids in the central nervous system, which will eventually induce vari-ous mental illnesses like depression, etc. This article reviews the research advancement in the relationship between MTHFR-677C/T polymorphism and depression in recent years on the basis of MTHFR gene mutation and function, lack of folic acid, elevated plasma homocysteine levels and the MTHFR-C677T polymor-phism. Based on which we hope to bring new ideas about treat-ment of depression.
ABSTRACT
Polo-like kinase 1(PLK1)is a serine/threonine kinase which is highly conserved, and its activity is elevated in many human tumor cell lines.Lots of reports have shown that PLK1 is critical for all stages of mitosis.The newest report finds that PLK1 is required for DNA synthesis, maintenance of DNA integrity, and prevention of cell death.PLK1 physically binds to the tumor suppressor p53 in mammalian cultured cells, and inhibits its transactivation activity as well as its function in activate checkpoint protein and its pro-apoptotic function.Also PLK1 is involved in the development of tumors, and Polo-like kinase1(PLK1)regulates IFN induction by MAVS, breakdown the innate immunity. Various of inhibitors of PLK1 show the feature of high performance and low toxicity, suggesting that PLK1 may be a feasible target for cancer therapy and immunity therapy.