Abstract A45: High CDC2_1 activatory functions and mechanisms in lung adenocarcinoma

Abstract

Abstract In order to study high CDC2_1 feedback-interactive cell cycle mechanism in lung adenocarcinoma, high CDC2_1 feedback-interactive multidimensional molecular network was constructed from mutual positive correlation of the overlapping with CDC2_1 direct activatory relationship by GRNInfer and Pearson correlation coefficient CC ≥0.25 in lung adenocarcinoma (GSE7670 from Taiwan samples). Our result showed a loop from TOP2A_2 to CKS1B to RRM2_1, respectively; There are interactions among TOP2A_2 to CKS1B to RRM2_1, respectively. Therefore, we proposed high CDC2_1 feedback-interactive TOP2A_2 interactive CKS1B interactive RRM2_1 loop. Based on GO, KEGG, GenMAPP, BioCarta and disease databases, RRM2_1, TOP2A_2, CKS1B knowledge included DNA replication, cytoplasm, protein-binding, nucleoplasm, cell cycle, cell division, etc. We further put forward high CDC2_1 feedback-interactive cell cycle in lung adenocarcinoma. In order to study high CDC2_1 activated-upstream mitosis mechanism in lung adenocarcinoma, high CDC2_1 activated-upstream multidimensional molecular network was constructed. Our result showed interactions among NCAPG_1 to SPAG5 to NDC80, respectively. Therefore, we proposed high CDC2_1 activated-upstream NCAPG_1 to SPAG5 to NDC80 interaction. Based on GO, KEGG, GenMAPP, BioCarta and disease databases, NCAPG_1, SPAG5, NDC80 knowledge included M phase, nucleus, cytoplasm, protein-binding, mitosis, condensed chromosome kinetochore, spindle organization and biogenesis, phosphoinositide-mediated signaling, condensin complex, mitotic chromosome condensation, spindle microtubule, cytokinesis, chromosome, pericentric region, mitotic sister chromatid segregation, etc. We further put forward high CDC2_1 activated-upstream mitosis in lung adenocarcinoma. In order to study high CDC2_1 activating-downstream mitosis mechanism in lung adenocarcinoma, high CDC2_1 activating-downstream multidimensional molecular network was constructed. Our result showed mutual interaction among EPN3, NUSAP1_1, PRC1. Therefore, we proposed high CDC2_1 activating-downstream EPN3/NUSAP1_1/PRC1 complex. Based on GO, KEGG, GenMAPP, BioCarta and disease databases, NCAPG_1, SPAG5, NDC80 knowledge included nucleus, cytoplasm, lipid-binding, cell cycle, cell division, cytokinesis, cytoplasmic vesicle, microtubule, DNA-binding, cytokinesis after mitosis, mitotic chromosome condensation, establishment of mitotic spindle localization, protein-binding, mitotic spindle elongation, Embryonic Stem Cell, microtubule cytoskeleton, etc. We further put forward high CDC2_1 activating-downstream mitosis in lung adenocarcinoma. High CDC2_1 feedback-interactive, activated-upstream and activating-downstream molecular networks were reverse-verified by the corresponding high CDC2_1 repressive network in lung adenocarcinoma, activatory and repressive in human normal adjacent lung adenocarcinoma tissues, respectively. Citation Format: Lin Wang, Juxiang Huang, Minghu Jiang, Qingchun Chen, Zhenfu Jiang, Haitao Feng. High CDC2_1 activatory functions and mechanisms in lung adenocarcinoma. [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; 2015 Nov 5-9; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Ther 2015;14(12 Suppl 2):Abstract nr A45.