Role of Myeloid Cell Leukemia-1 in Cell Growth of Squamous Cell Carcinoma
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- Nagata Masahide
- Department of Pharmacology, Graduate School of Dentistry, Osaka University, Japan The First Department of Oral and Maxillofacial Surgery, Graduate School of Dentistry, Osaka University, Japan
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- Wada Koichiro
- Department of Pharmacology, Graduate School of Dentistry, Osaka University, Japan
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- Nakajima Atsushi
- Division of Gastroenterology, Yokohama City University School of Medicine, Japan
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- Nakajima Noriko
- Department of Pathology, National Institute of Infectious Diseases, Japan
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- Kusayama Morio
- Department of Pharmacology, Graduate School of Dentistry, Osaka University, Japan The First Department of Oral and Maxillofacial Surgery, Graduate School of Dentistry, Osaka University, Japan
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- Masuda Tomotake
- The First Department of Oral and Maxillofacial Surgery, Graduate School of Dentistry, Osaka University, Japan
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- Iida Seiji
- The First Department of Oral and Maxillofacial Surgery, Graduate School of Dentistry, Osaka University, Japan
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- Okura Masaya
- The First Department of Oral and Maxillofacial Surgery, Graduate School of Dentistry, Osaka University, Japan
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- Kogo Mikihiko
- The First Department of Oral and Maxillofacial Surgery, Graduate School of Dentistry, Osaka University, Japan
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- Kamisaki Yoshinori
- Department of Pharmacology, Graduate School of Dentistry, Osaka University, Japan
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Abstract
Myeloid cell leukemia-1 (Mcl-1), a member of the B-cell lymphoma-2 (Bcl-2) family, has been reported to be a critical survival factor in hematopoietic cells, yet little data exists for a role of Mcl-1 in human oral squamous cell carcinoma (SCC). A high level expression of Mcl-1 was observed in tumor cells of human primary SCC, lymph node metastasis tissues, and SCC cell lines. We manipulated expression of Mcl-1 protein in SCC cells by small interfering RNA (siRNA) for Mcl-1 and observed that Mcl-1 siRNA inhibited the growth of SCCs accompanied with apoptosis. Combination therapy of Mcl-1 siRNA and anti-tumor drug drastically inhibited the cell growth in comparison to that in each single treatment. In addition, phosphorylation of focal adhesion kinase (FAK) was decreased by treatment with Mcl-1 siRNA, resulting in decreases in phosphorylation of MEK1/2 and MAPK. The cell growth inhibition caused by knockdown of Mcl-1 was suggested to be mainly a result of suppression of proliferation via the inhibition of intracellular FAK/MAPK signaling pathways. These results imply a potentially important and novel role of the inhibition of Mcl-1 function by the use of specific siRNA in the treatment of SCC.<br>
Journal
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- Journal of Pharmacological Sciences
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Journal of Pharmacological Sciences 110 (3), 344-353, 2009
The Japanese Pharmacological Society
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Details
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- CRID
- 1390001205178561920
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- NII Article ID
- 10025737800
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- NII Book ID
- AA11806667
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- ISSN
- 13478648
- 13478613
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- NDL BIB ID
- 10283409
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- Text Lang
- en
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- Data Source
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- JaLC
- NDL
- Crossref
- CiNii Articles
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- Abstract License Flag
- Disallowed