TY - JOUR
T1 - Effect of CLN3 silencing by RNA interference on the proliferation and apoptosis of human colorectal cancer cells
AU - Zhu, Xinguo
AU - Huang, Zhilong
AU - Chen, Yan
AU - Zhou, Jian
AU - Hu, Shuiqing
AU - Zhi, Qiaoming
AU - Song, Shiduo
AU - Wang, Yanan
AU - Wan, Daiwei
AU - Gu, Wen
AU - Zhou, Hao
AU - Zhang, Bo
AU - Cao, Wei
AU - He, Songbing
N1 - Funding Information:
This study was supported by Project of Nature Science Foundation of China (81201905, 81100023), China Postdoctoral Science Foundation (2013M540374), Nature Science Research Grants in University of Jiangsu Province of China (12KJB320009), Project of Medical Science and Technology Development Foundation of Jiangsu Province of China (H201209), Innovation Program of Shanghai Municipal Education Commission (12YZ050), Shanghai Postdoctoral Scientific Program of China (13R21415200) and Science and Technology Research Project of in Science and Technology Bureau of Suzhou City of China (SYS201220) and sponsored by Government Overseas Scholarship from Department of Education of Jiangsu Province of China.
PY - 2014/4
Y1 - 2014/4
N2 - Apoptosis constitutes a system for the removal of aged, or damaged cells, which is regulated by the interplay of pro-apoptotic and antiapoptotic proteins. Previous study has shown that Juvenile Batten disease protein, CLN3, is antiapoptotic gene in NT2 neuronal precursor cells and a few types of cancers. However, in colorectal cancer, whether CLN3 also play its antiapoptotic role and the effect of targeted controlling CLN3 on the biological behavior of human colorectal cancer cell is unknown. We employed the sequence-specific siRNA silencing the CLN3 gene and investigated its effects on growth and apoptosis of colorectal cancer HCT116 cells, which has highest elevation of CLN3 expression among four colorectal cancer cell lines. After CLN3 specific siRNA transfection, mRNA and protein expression levels of CLN3 in HCT116 cells were noticeably decreased. Moreover, CLN3-siRNA inhibited the proliferation of colorectal cancer cells, promoted their apoptosis and induced G0/G1 cell cycle arrest. Our current study demonstrated that CLN3 was expressed in colorectal cancer cells at a high frequency. Moreover, CLN3 down-regulation with RNA interference can inhibit proliferation, apoptosis, and cell cycle progression of colorectal cancer cells. Our study represented a potential new approach to understanding the role of CLN3 in cancer and provides a potential novel strategy colorectal cancer therapy.
AB - Apoptosis constitutes a system for the removal of aged, or damaged cells, which is regulated by the interplay of pro-apoptotic and antiapoptotic proteins. Previous study has shown that Juvenile Batten disease protein, CLN3, is antiapoptotic gene in NT2 neuronal precursor cells and a few types of cancers. However, in colorectal cancer, whether CLN3 also play its antiapoptotic role and the effect of targeted controlling CLN3 on the biological behavior of human colorectal cancer cell is unknown. We employed the sequence-specific siRNA silencing the CLN3 gene and investigated its effects on growth and apoptosis of colorectal cancer HCT116 cells, which has highest elevation of CLN3 expression among four colorectal cancer cell lines. After CLN3 specific siRNA transfection, mRNA and protein expression levels of CLN3 in HCT116 cells were noticeably decreased. Moreover, CLN3-siRNA inhibited the proliferation of colorectal cancer cells, promoted their apoptosis and induced G0/G1 cell cycle arrest. Our current study demonstrated that CLN3 was expressed in colorectal cancer cells at a high frequency. Moreover, CLN3 down-regulation with RNA interference can inhibit proliferation, apoptosis, and cell cycle progression of colorectal cancer cells. Our study represented a potential new approach to understanding the role of CLN3 in cancer and provides a potential novel strategy colorectal cancer therapy.
KW - Apoptosis
KW - CLN3
KW - Colorectal cancer
KW - Proliferation
KW - RNA interference
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U2 - 10.1016/j.biopha.2013.12.010
DO - 10.1016/j.biopha.2013.12.010
M3 - Article
C2 - 24556023
AN - SCOPUS:84899053888
SN - 0753-3322
VL - 68
SP - 253
EP - 258
JO - Biomedicine and Pharmacotherapy
JF - Biomedicine and Pharmacotherapy
IS - 3
ER -