Overexpression of N-terminal kinase like gene promotes tumorigenicity of hepatocellular carcinoma by regulating cell cycle progression and cell motility

• المؤلفون الرئيسيون: Wang, J, Liu, M, Chen, L, Chan, T.H.M, Jiang, L, Yuan, Y.-F, Guan, X.-Y
• مؤلفون آخرون: ANATOMY
• التنسيق: مقال
• منشور في: 2020
• الموضوعات: agar; cyclin D1; dynamin II; F actin; guanosine triphosphatase; n terminal kinase like protein; protein; protein Cdc42; protein p53; Rac1 protein; unclassified drug; CHD1L protein, human; DNA binding protein; DNA helicase; DNM2 protein, human; dynamin; SCYL1 protein, human; transcription factor; adult; amino terminal kinase like gene; animal cell; animal experiment; animal model; animal tissue; apoptosis; Article; cancer prognosis; carcinogenesis; carcinogenicity; cell cycle progression; cell division; cell growth; cell motility; CHD1L oncogene; chromatin immunoprecipitation; chromosome segregation; colony formation; controlled study; correlation analysis; cytokinesis; enzyme phosphorylation; female; G1 phase cell cycle checkpoint; gene; gene expression; gene overexpression; human; human tissue; lamellipodium; liver cell carcinoma; major clinical study; male; mass spectrometry; mitosis; mouse; mutation; nonhuman; nude mouse; oncogene; phenotype; promoter region; real time polymerase chain reaction; animal; biosynthesis; cell cycle; cell motion; cell proliferation; enzymology; genetics; liver tumor; metabolism; middle aged; pathology; physiology; tumor cell line; xenograft; Animals; Apoptosis; Carcinoma, Hepatocellular; Cell Cycle; Cell Line, Tumor; Cell Movement; Cell Proliferation; DNA Helicases; DNA-Binding Proteins; Dynamins; Female; Gene Expression; Heterografts; Humans; Liver Neoplasms; Male; Mice; Middle Aged; Transcription Factors
• الوصول للمادة أونلاين: https://scholarbank.nus.edu.sg/handle/10635/180963

10.18632/oncotarget.2730