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Biomed Pharmacother. 2014 Apr;68(3):253-8. doi: 10.1016/j.biopha.2013.12.010. Epub 2014 Jan 15.

Effect of CLN3 silencing by RNA interference on the proliferation and apoptosis of human colorectal cancer cells.

Author information

  • 1Department of General Surgery, the First Affiliated Hospital of Soochow University, 188, Shizi Street, 215006 Suzhou, Jiangsu Province, China.
  • 2Department of Clinical Laboratories, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, 200011 Shanghai, China.
  • 3Department of Clinical Laboratory, Suzhou Municipal Hospital, the Affiliated Hospital of Nanjing Medical University, 215006 Suzhou, China.
  • 4Department of General Surgery, the First Affiliated Hospital of Sun Yat-sen University, 510000 Guangzhou, China.
  • 5Department of General Surgery, Zhangjiagang First People Hospital, 215600 Suzhou, China.
  • 6Department of General Surgery, the First Affiliated Hospital of Soochow University, 188, Shizi Street, 215006 Suzhou, Jiangsu Province, China; Shanghai Jiao Tong University School of Medicine, 200025 Shanghai, China; Washington University School of Medicine, St Louis, Missouri 63110, USA. Electronic address: captain_hsb@163.com.

Abstract

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.

KEYWORDS:

Apoptosis; CLN3; Colorectal cancer; Proliferation; RNA interference

PMID:
24556023
DOI:
10.1016/j.biopha.2013.12.010
[PubMed - indexed for MEDLINE]
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