期刊
HUMAN CELL
卷 28, 期 4, 页码 167-174出版社
SPRINGER JAPAN KK
DOI: 10.1007/s13577-015-0117-3
关键词
Pancreatic cancer; Slug; CD133; Chemoresistance; Gemcitabine
类别
资金
- JSPS KAKENHI from Ministry of Education, Culture, Sports, Science and Technology, Japan [25293288]
- Grants-in-Aid for Scientific Research [25293288] Funding Source: KAKEN
CD133-positive pancreatic cancer is correlated with unfavorable survival despite current development of therapy. Slug acts as a master regulator of epithelial-mesenchymal transition (EMT) which is the essential process in cancer progression. The aim of this study was to investigate the role of Slug in gemcitabine treatment for CD133-positive pancreatic cancer cells. We used a previously established pancreatic cancer cell line expressing high level of CD133 (Capan-1M9), which also expresses high level of Slug. We generated Slug knock-down sub-clone (shSlug M9) from this cell line, and compared expression of EMT-related genes, migration, invasion and gemcitabine resistance between two cell lines. Slug knockdown in CD133-positive pancreatic cancer cell line led to the reduction of migration and invasion ability. Furthermore, Slug knock-down sensitized CD133-positive pancreatic cancer cell line to gemcitabine. These results suggest that Slug plays an important role in not only invasion ability through EMT but also gemcitabine resistance of CD133-positive pancreatic cancer cells.
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