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Hindi Research Article
Overexpression of the Novel Tumor Suppressor Gene FUS1 Suppresses the Growth of Small Cell Lung Cancer Cells
Cancer Cells Roza Zandi1,2*, Kai Xu1, Hans S. Poulsen2, Jack A. Roth1 and Lin Ji11Department of Thoracic and Cardiovascular Surgery, The University of Texas, M.D. Anderson Cancer Center, Houston, Texas, USA
2Department of Radiation Biology, The Finsen Centre section 6321, Copenhagen University Hospital, Copenhagen, Denmark
- *Corresponding Author:
- Roza Zandi
Department of Radiation Biology
The Finsen Centre section 6321
Copenhagen University Hospital
DK2100 Copenhagen, Denmark
Tel: 45 35456329
Fax: 45 35456301
E-mail: roza@zandi.dk, roza@rh.dk
Received Date: September 30, 2011; Accepted Date: November 25, 2011; Published Date: December 03, 2011
Citation: Zandi R, Xu K, Poulsen HS, Roth JA, Ji L (2011) Overexpression of the Novel Tumor Suppressor Gene FUS1 Suppresses the Growth of Small Cell Lung Cancer Cells. J Clinic Experiment Pathol S5:001. doi: 10.4172/2161-0681.S5-001
Copyright: © 2011 Zandi R, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
FUS1, also known as tumor suppressor candidate 2 (TUSC2), is a novel candidate tumor suppressor gene (TSG) frequently inactivated in human lung cancer. Loss of FUS1 protein expression is found in almost all small cell lung cancer (SCLC) cell lines and tumor specimens. Therefore, restoration of normal FUS1 function by gene transfer could serve as a potential therapeutic strategy for the treatment of SCLC. Here we investigated the effect of exogenous expression of FUS1 by plasmid-mediated gene transfer on tumor cell growth and apoptosis induction in FUS1-defective SCLC cells. Transfection of SCLC cells with wild-type FUS1 (wt-FUS1) showed in vitro growth inhibition and a marked suppression of colony formation compared to cells transfected with an empty vector (EV) or a myristoylation-defect mutant FUS1 (mt-FUS1). Forced expression of wt-FUS1 also increased the apoptotic cell population at Sub-G0/G1 in SCLC cells compared to EV- and mt-FUS1-transfected controls, which was associated with a decreased level of pro-caspase-3 and an increased level of PARP cleavage. Our results demonstrate the potential tumor suppression function of FUS1 in SCLC cells and suggest that FUS1-mediated gene therapy could be a useful therapeutic strategy for the treatment of SCLC.
