Our findings concluded that BCH showed good inhibition on the HCC proliferation and colony formation, which attributed to cell cycle arrest by BCH at G1 phase through impairing the expression of cyclinD1, cyclinE, and cdc2 and downregulated the phosphorylation of Akt, mTOR, and ERK.
We also show that RMP depletion induced the G(2) arrest of HCC cells characterized by the decreased expression of Cdk1 and Cyclin B. Tumor formation assays further confirmed the in vivo requirement of RMP during HCC growth.
Surprisingly, ZWINT, CENPA, RACGAP1, PLK1, NCAPG, OIP5, CDCA8, PRC1, and CDK1 were identified statistically as hub genes in the blue module, which were closely implicated in pathological T stage and histologic grade of HCC.
<b>Results:</b> We found that CDK1 was frequently augmented in up to 46% (18/39) of HCC tissues, which was significantly associated with poor overall survival (p=0.008).
These results suggest that the prognostic predictive capacities of these gene signatures are reproducible and that CDK1 is a potential prognostic biomarker or therapeutic target for HCC patients.
Flow cytometry showed that genistein, but not biochanin-A or daidzein, induced progressive and sustained accumulation of hepatoma cancer cells in the G2/M phase as a result of inhibition of Cdc2 kinase activity.
Further studies showed that miR-582-5p regulated the progression of HCC through directly inhibiting the expression of CDK1 and AKT3, and indirectly inhibiting the expression of cyclinD1.
We identified six mRNAs (DPYSL4, HOMER1, ABCB6, CENPA, CDK1, STMN1) significantly associated with overall survival in the Cox proportional regression model for hepatocellular carcinoma.
The PFTK1 gene encodes a cdc2-related serine/threonine protein kinase that has been shown to confer cell migratory properties in hepatocellular carcinoma (HCC).
By counteracting C53, pre-S2 LHBs promotes Cdk1 activation and mitotic entry in unperturbed cell cycle progression and delays the function of Chk1, which may be a novel potential mechanism for HBV-induced hepatocellular carcinoma (HCC).
These observations were further confirmed in vivo by the reciprocal control of TIS21 expression and FoxM1 phosphorylation in the diethylnitrosamine-induced HCCs and TIS21(-/-) mouse embryonic fibroblast (MEF), in addition to increased expression of cyclin B1 and cdk1 activity.
Furthermore, cell cycle and p53 signaling pathways may play vital mediatory roles; CDK1 may play crucial roles in HCC transformed from cirrhosis via cell cycle and p53 signaling pathways, and RRM2 might be involved in HCC transformed from cirrhosis via the p53 signaling pathway.
The results demonstrated that KPNA2 expression was significantly upregulated in HCC tumor tissues compared with liver tissues and was associated with cyclin B2 (CCNB2) and cyclin-dependent kinase 1 (CDK1) expression.
Our findings show that the upregulation of BMP4 and BMPR1A in HCC promotes the proliferation and metastasis of HCC cells and that CDK1 and cyclin B1 are important SMAD-independent molecular targets in BMP4 signaling pathways, during the HCC tumorigenesis.
Millepachine, a novel chalcone, induces G2/M arrest by inhibiting CDK1 activity and causing apoptosis via ROS-mitochondrial apoptotic pathway in human hepatocarcinoma cells in vitro and in vivo.
Bioinformatics analysis identified 469 related genes and further analysis supported a hypothesis that LINC00665 regulates pathways in the cell cycle to facilitate the development and progression of HCC through ten identified core genes: CDK1, BUB1B, BUB1, PLK1, CCNB2, CCNB1, CDC20, ESPL1, MAD2L1, and CCNA2.
Although E2F8 and E2F7 perform complementary and overlapping functions in many cell metabolisms, E2F8, but not E2F7, overexpresses remarkably in hepatocellular carcinoma (HCC) to facilitate the HCC occurrence and development <i>via</i> activating a E2F1/ Cyclin D1 signaling pathway to regulate the G1- to S-phase transition of cell cycle progression or transcriptionally suppressing CDK1 to induce hepatocyte polyploidization.