Journal Basic Info

  • Impact Factor: 2.709**
  • H-Index: 11 
  • ISSN: 2474-1663
  • DOI: 10.25107/2474-1663
**Impact Factor calculated based on Google Scholar Citations. Please contact us for any more details.

Major Scope

  •  Melanoma/Skin Cancer
  •  Blood Cancer
  •  Immunology
  •  Urological Cancers
  •  Palliative Care
  •  Pancreatic Cancer
  •  Lung Cancers
  •  Carcinomas


Citation: Clin Oncol. 2016;1(1):1015.DOI: 10.25107/2474-1663.1015

Over-Expression of Cofilin-1 Suppressed Mobility of Lung Cancer Cells is Associated with Down-Regulation of SNAIL-1 and Induction of Let-7

Wang CY, Tsai CH, Chang CY, Liao MJ, Liu RS and Lee YJ

Department of Medical Imaging, Cheng Hsin General Hospital, Taiwan
Departments of Biomedical Imaging and Radiological Sciences, National Yang-Ming University, Taiwan
Department of Nuclear Medicine, National PET/Cyclotron Center, Taiwan
Molecular and Genetic Imaging Core, Medical School, National Yang-Ming University, Taiwan
Biophotonics & Molecular Imaging Research Center (BMIRC), National Yang-Ming University, Taiwan

*Correspondance to: Yi-Jang Lee 

 PDF  Full Text Research Article | Open Access


Metastatic lung cancer means the spread of cancer from the primary site to nearby structures or distant organs. Epithelial-mesenchymal transition (EMT) is an important mechanism to be associated with metastasis. Suppression of EMT may prevent the cancer metastasis. We previously found that over-expression of cofilin-1, an actin binding protein belongs to the actin depolymerizing factor (ADF)/cofilin family leads to morphological change and inhibition of invasion of human non-small cells lung cancer (NSCLC). This effect is associated with up-regulation of the tumor suppressive let-7 microRNA through TWIST-1 transcription factor, an important biomarker of EMT. Here we investigated whether other EMT related molecules would be affected by overexpressed cofilin-1. Over-expression of cofilin-1 in human H1299 lung cancer cells also suppressed SNAIL-1 transcription factors, but E-cadherin and N-cadherin were not significantly affected. Importantly, over-expression of cofilin-1 induced let-7 could be suppressed by enforced expression of SNAIL-1, suggesting that EMT related transcription factors can be suppressed by over-expressed cofilin-1 to induce let-7 expression. However, over-expression of cofilin-1 may not suppress EMT. To monitor the effects of cofilin-1 and let-7 on lung cancer migration in vivo, we established a multiple reporter genes transduced lung cancer cell line that can be detected using the reporter gene imaging. The cofilin-1 induced let-7 was suppressed by transfection of locked nucleic acid (LNA) to inhibit let-7. Compared to normal lung cancer cells, over-expression of cofilin-1 suppressed the lung cancer migration, but simultaneously transfection of LNA recovered their migration ability to lungs in small animals. Taken together, over-expression of cofilin-1 can suppress the invasion and migration of lung cancer cells through up-regulation of let-7 in vitro and in vivo. Additionally, cofilin-1 may regulate EMT related transcription factors but not the whole EMT mechanism.


Cofilin-1; SNAIL-1; let-7; EMT; Reporter gene imaging; Locked nucleic acid

Cite the Article:

Wang CY, Tsai CH, Chang CY, Liao MJ, Liu RS, Lee YJ. Over-Expression of Cofilin-1 Suppressed Mobility of Lung Cancer Cells is Associated with DownRegulation of SNAIL-1 and Induction of Let-7. Clin Oncol. 2016; 1: 1015.

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