Please use this identifier to cite or link to this item: https://doi.org/10.18632/oncotarget.12251
Title: Targeting SALL4 by entinostat in lung cancer
Authors: Yong, K.J 
Li, A
Ou, W.-B
Hong, C.K.Y
Zhao, W
Wang, F
Tatetsu, H
Yan, B
Qi, L 
Fletcher, J.A
Yang, H 
Soo, R 
Tenen, D.G 
Chai, L
Keywords: entinostat
epidermal growth factor receptor
SALL4 protein
somatomedin C receptor
tumor protein
unclassified drug
antineoplastic agent
benzamide derivative
entinostat
histone deacetylase inhibitor
pyridine derivative
SALL4 protein, human
small interfering RNA
transcription factor
adult
Article
cancer growth
cancer survival
controlled study
disease activity
drug effect
drug mechanism
drug targeting
female
human
lung cancer
lung carcinogenesis
major clinical study
male
molecular pathology
protein determination
protein expression
protein function
RNA interference
signal transduction
survival rate
animal
antagonists and inhibitors
cell survival
disease model
drug screening
gene expression
genetics
lung tumor
mouse
tumor cell line
Animals
Antineoplastic Agents
Benzamides
Cell Line, Tumor
Cell Survival
Disease Models, Animal
Gene Expression
Histone Deacetylase Inhibitors
Humans
Lung Neoplasms
Mice
Pyridines
RNA Interference
RNA, Small Interfering
Transcription Factors
Xenograft Model Antitumor Assays
Issue Date: 2016
Citation: Yong, K.J, Li, A, Ou, W.-B, Hong, C.K.Y, Zhao, W, Wang, F, Tatetsu, H, Yan, B, Qi, L, Fletcher, J.A, Yang, H, Soo, R, Tenen, D.G, Chai, L (2016). Targeting SALL4 by entinostat in lung cancer. Oncotarget 7 (46) : 75425-75440. ScholarBank@NUS Repository. https://doi.org/10.18632/oncotarget.12251
Abstract: The overall survival of lung cancer patients remains dismal despite the availability of targeted therapies. Oncofetal protein SALL4 is a novel cancer target. We herein report that SALL4 was aberrantly expressed in a subset of lung cancer patients with poor survival. SALL4 silencing by RNA interference or SALL4 peptide inhibitor treatment led to impaired lung cancer cell growth. Expression profiling of SALL4-knockdown cells demonstrated that both the EGFR and IGF1R signaling pathways were affected. Connectivity Map analysis revealed the HDAC inhibitor entinostat as a potential drug in treating SALL4-expressing cancers, and this was confirmed in 17 lung cancer cell lines. In summary, we report for the first time that entinostat can target SALL4-positive lung cancer. This lays the foundation for future clinical studies evaluating the therapeutic efficacy of entinostat in SALL4-positive lung cancer patients.
Source Title: Oncotarget
URI: https://scholarbank.nus.edu.sg/handle/10635/174105
ISSN: 19492553
DOI: 10.18632/oncotarget.12251
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