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miR-27a is highly expressed in H1650 cancer stem cells and regulates proliferation, migration, and invasion


1 Key Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China
2 Key Laboratory of Systems Biomedicine Ministry of Education, Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai, China

Correspondence Address:
Zhixue Liu,
Room 2010, New Life Building, 320 Yueyang Road, Shanghai
China
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Source of Support: None, Conflict of Interest: None

Background: Cancer stem cells (CSCs) are responsible for tumor relapse after chemotherapy and radiotherapy in non-small cell lung cancer (NSCLC). The aim of this study is to explore the profile and role of microRNA (miRNA) in CSC of NSCLC. Materials and Methods: We studied the expression of stem cell marker in side population cells and serum-free cultured spheres of NSCLC. We identified that CD133+ CD34 cells are NSCLC stem cell. We isolated CD133+ CD34 cells and CD133 CD34+ cells with MicroBead Kit. We verified that H1650 CD133+ CD34 cells have CSC characteristics with doxorubicin, radiation, and xenograft. We studied miRNA expression profile in H1650 and HCC827 CD133+ CD34 cells with microarray analysis. We detected proliferation, migration, and invasion with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, scratch test, and Transwell chamber invasion assay, respectively. Results: CD133 and CD34 are CSC markers in H1650. We demonstrated that H1650 CD133+ CD34 cells have CSC characteristics and found that miR-27a was highly expressed in H1650 CD133+ CD34 cells. In addition, we showed that miR-27a regulates proliferation, migration, and invasion in H1650 cell line and demonstrated that miR-27a expression was positively related to epidermal growth factor receptor in NSCLC cell lines. Conclusion: CD133+ CD34 is a CSC marker in H1650. miR-27a is highly expressed in H1650 CSCs and regulates cancer development in H1650. miR-27a may be a potential target for NSCLC therapy.


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