Research Papers:
Friend leukemia virus integration 1 activates the Rho GTPase pathway and is associated with metastasis in breast cancer
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Abstract
Wei Song1, Wei Li1, Lingyu Li1, Shilin Zhang1,2, Xu Yan1, Xue Wen1, Xiaoying Zhang1, Huimin Tian1, Ailing Li3, Ji-Fan Hu1,2, Jiuwei Cui1
1Cancer Center, the First Hospital of Jilin University, Changchun, China
2Stanford University Medical School, VA Palo Alto Health Care System, Palo Alto, CA, USA
3Institute of Basic Medical Sciences, National Center of Biomedical Analysis, Beijing, China
Correspondence to:
Jiuwei Cui, e-mail: [email protected]
Jifan Hu, e-mail: [email protected]
Keywords: FLI1, breast cancer, metastasis, oncogene, RhoA pathway
Abbreviations: BC: breast cancer; FLI1: friend leukemia virus integration 1; ROCK: rho-associated coiled coil-containing protein kinase; shRNA: short hairpin RNA; siRNA: small interfering RNA
Received: May 01, 2015 Accepted: June 11, 2015 Published: June 24, 2015
ABSTRACT
Breast cancer is the most prevalent malignant disease in women worldwide. In patients with breast cancer, metastasis to distant sites directly determines the survival outcome. However, the molecular mechanism underlying metastasis in breast cancer remains to be defined. In this report, we found that Friend leukemia virus integration 1 (FLI1) proto-oncogene was differentially expressed between the aggressive MDA-MB231 and the non-aggressive MCF-7 breast cancer cells. Congruently, immunohistochemical staining of clinical samples revealed that FLI1 was overexpressed in breast cancers as compared with the adjacent tissues. The abundance of FLI1 protein was strongly correlated with the advanced stage, poor differentiation, and lymph node metastasis in breast cancer patients. Knockdown of FLI1 with small interfering RNAs significantly attenuated the potential of migration and invasion in highly metastatic human breast cancer cells. FLI1 oncoprotein activated the Rho GTPase pathway that is known to play a role in tumor metastasis. This study for the first time identifies FLI1 as a clinically and functionally important target gene of metastasis, providing a rationale for developing FLI1 inhibitors in the treatment of breast cancer.
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