Membrane Protein Metabolism in UNG-Activated NCAPH and RFC4 Subnetworks for Viral HCC|blood Cancer Development Via Inside-Out Microtubule Binding

Abstract Background: Our aim is to compute NCAPH and RFC4 subnetworks containing CDKN3 (feedback) for the novel molecular and cellular mechanisms of HCC (HBV or HCV) related cancer development from high UNG-activated upstream network.Methods: Non-SMC condensin I complex subunit H (NCAPH) and replication factor C subunit 4 (RFC4) common molecular and knowledge subnetworks containing cyclin-dependent kinase inhibitor 3-CDKN3 (feedback) related to cancer by references were identified in HCC (HBV or HCV), based on our established significant high expression uracil DNA glycosylase (UNG)-activated upstream Gene (protein) reconstruction network inference (GRNInfer) and Database for Annotation, Visualization and Integrated Discovery (DAVID).Results: Our results show the common molecules MAPT interaction with CDKN3 with RRM2 with HIST1H3H from UNG-activated upstream GRNInfer database; The common biological process and molecular function of MAPT as microtubule binding; HIST1H3H as cellular protein metabolic process from UNG-activated upstream DAVID database; The common cellular component of UNG, NCAPH, CDKN3, RRM2, HIST1H3H at nucleus; NCAPH, HIST1H3H at membrane; The common tissue distributions of NCAPH and RFC4 in Leukemiapromyelocytic(hl60), leukemialymphoblastic(molt4), etc.Conclusions: We propose and mutual positively verify membrane protein metabolism in UNG-activated NCAPH and RFC4 subnetworks for viral HCC|blood cancer development via inside-out microtubule binding.