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.