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

10.18632/oncotarget.2730

Saved in:

Bibliographic Details
Main Authors:	Wang, J, Liu, M, Chen, L, Chan, T.H.M, Jiang, L, Yuan, Y.-F, Guan, X.-Y
Other Authors:	ANATOMY
Format:	Article
Published:	2020
Subjects:	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
Online Access:	https://scholarbank.nus.edu.sg/handle/10635/180963
Tags:	Add Tag No Tags, Be the first to tag this record!
Institution:	National University of Singapore

id	sg-nus-scholar.10635-180963
record_format	dspace
spelling	sg-nus-scholar.10635-1809632024-04-08T14:34:01Z Overexpression of N-terminal kinase like gene promotes tumorigenicity of hepatocellular carcinoma by regulating cell cycle progression and cell motility Wang, J Liu, M Chen, L Chan, T.H.M Jiang, L Yuan, Y.-F Guan, X.-Y ANATOMY CANCER SCIENCE INSTITUTE OF SINGAPORE 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 cell carcinoma 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 10.18632/oncotarget.2730 Oncotarget 6 3 1618-1630 2020-10-27T05:53:24Z 2020-10-27T05:53:24Z 2015 Article Wang, J, Liu, M, Chen, L, Chan, T.H.M, Jiang, L, Yuan, Y.-F, Guan, X.-Y (2015). Overexpression of N-terminal kinase like gene promotes tumorigenicity of hepatocellular carcinoma by regulating cell cycle progression and cell motility. Oncotarget 6 (3) : 1618-1630. ScholarBank@NUS Repository. https://doi.org/10.18632/oncotarget.2730 19492553 https://scholarbank.nus.edu.sg/handle/10635/180963 Attribution 4.0 International http://creativecommons.org/licenses/by/4.0/ Unpaywall 20201031
institution	National University of Singapore
building	NUS Library
continent	Asia
country	Singapore Singapore
content_provider	NUS Library
collection	ScholarBank@NUS
topic	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 cell carcinoma 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
spellingShingle	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 cell carcinoma 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 Wang, J Liu, M Chen, L Chan, T.H.M Jiang, L Yuan, Y.-F Guan, X.-Y Overexpression of N-terminal kinase like gene promotes tumorigenicity of hepatocellular carcinoma by regulating cell cycle progression and cell motility
description	10.18632/oncotarget.2730
author2	ANATOMY
author_facet	ANATOMY Wang, J Liu, M Chen, L Chan, T.H.M Jiang, L Yuan, Y.-F Guan, X.-Y
format	Article
author	Wang, J Liu, M Chen, L Chan, T.H.M Jiang, L Yuan, Y.-F Guan, X.-Y
author_sort	Wang, J
title	Overexpression of N-terminal kinase like gene promotes tumorigenicity of hepatocellular carcinoma by regulating cell cycle progression and cell motility
title_short	Overexpression of N-terminal kinase like gene promotes tumorigenicity of hepatocellular carcinoma by regulating cell cycle progression and cell motility
title_full	Overexpression of N-terminal kinase like gene promotes tumorigenicity of hepatocellular carcinoma by regulating cell cycle progression and cell motility
title_fullStr	Overexpression of N-terminal kinase like gene promotes tumorigenicity of hepatocellular carcinoma by regulating cell cycle progression and cell motility
title_full_unstemmed	Overexpression of N-terminal kinase like gene promotes tumorigenicity of hepatocellular carcinoma by regulating cell cycle progression and cell motility
title_sort	overexpression of n-terminal kinase like gene promotes tumorigenicity of hepatocellular carcinoma by regulating cell cycle progression and cell motility
publishDate	2020
url	https://scholarbank.nus.edu.sg/handle/10635/180963
_version_	1800914617745014784

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

Similar Items