CCNF is a potential pancancer biomarker and immunotherapy target

BackgroundCCNF catalyzes the transfer of ubiquitin molecules from E2 ubiquitin-conjugating enzymes to target proteins, thereby regulating the G1/S or G2/M transition of tumor cells. Thus far, CCNF expression and its potential as a pancancer biomarker and immunotherapy target have not been reported.MethodsTCGA datasets and the R language were used to analyze the pancancer gene expression, protein expression, and methylation levels of CCNF; the relationship of CCNF expression with overall survival (OS), recurrence-free survival (RFS), immune matrix scores, sex and race; and the mechanisms for posttranscriptional regulation of CCNF.ResultsCCNF expression analysis showed that CCNF mRNA expression was higher in cancer tissues than in normal tissues in the BRCA, CHOL, COAD, ESCA, HNSC, LUAD, LUSC, READ, STAD, and UCEC; CCNF protein expression was also high in many cancer tissues, indicating that it could be an important predictive factor for OS and RFS. CCNF overexpression may be caused by CCNF hypomethylation. CCNF expression was also found to be significantly different between patients grouped based on sex and race. Overexpression of CCNF reduces immune and stromal cell infiltration in many cancers. Posttranscriptional regulation analysis showed that miR-98-5p negatively regulates the expression of the CCNF gene.ConclusionCCNF is overexpressed across cancers and is an adverse prognostic factor in terms of OS and RFS in many cancers; this phenomenon may be related to hypomethylation of the CCNF gene, which could lead to cancer progression and worsen prognosis. In addition, CCNF expression patterns were significantly different among patients grouped by sex and race. Its overexpression reduces immune and stromal cell infiltration. miR-98-5p negatively regulates CCNF gene expression. Hence, CCNF is a potential pancancer biomarker and immunotherapy target

Suppression and azimuthal anisotropy of prompt and nonprompt J/psi production in PbPb collisions at root S-NN=2.76 TeV

The nuclear modification factor RAA and the azimuthal anisotropy coefficient v2 of prompt and nonprompt (i.e. those from decays of b hadrons) J/ψ mesons, measured from PbPb and pp collisions at sNN−−−√=2.76 TeV at the LHC, are reported. The results are presented in several event centrality intervals and several kinematic regions, for transverse momenta pT>6.5 GeV/c and rapidity |y|<2.4 , extending down to pT=3 GeV/c in the 1.6<|y|<2.4 range. The v2 of prompt J/ψ is found to be nonzero, but with no strong dependence on centrality, rapidity, or pT over the full kinematic range studied. The measured v2 of nonprompt J/ψ is consistent with zero. The RAA of prompt J/ψ exhibits a suppression that increases from peripheral to central collisions but does not vary strongly as a function of either y or pT in the fiducial range. The nonprompt J/ψ RAA shows a suppression which becomes stronger as rapidity or pT increases. The v2 and RAA of open and hidden charm, and of open charm and beauty, are compared

Virtual fragment screening for novel inhibitors of 6-phosphogluconate dehydrogenase

We report the identification of novel inhibitors of Trypanosoma brucei 6PGDH enzyme by virtual fragment screening