TY - JOUR
T1 - Localization of CD26/DPPIV in nucleus and its nuclear translocation enhanced by anti-CD26 monoclonal antibody with anti-tumor effect
AU - Yamada, Kohji
AU - Hayashi, Mutsumi
AU - Du, Wenlin
AU - Ohnuma, Kei
AU - Sakamoto, Michiie
AU - Morimoto, Chikao
AU - Yamada, Taketo
N1 - Funding Information:
This study was supported by the Program for Promotion of Fundamental Studies in Health Sciences of theNational Institute of Biomedical Innovation (07-17), a research grant from the Ministry of Education in Japan (20590354, 1770124), and Keio Gijuku Academic Development Funds, and a special grant-in-aid for innovative and collaborative research projects at Keio University.
PY - 2009/6/29
Y1 - 2009/6/29
N2 - Background: CD26 is a type II, cell surface glycoprotein known as dipeptidyl peptidase (DPP) IV. Previous studies have revealed CD26 expression in T cell leukemia/lymphoma and malignant mesothelioma, and an inhibitory effect of anti-CD26 monoclonal antibody (mAb) against the growth of CD26+ cancer cells in vitro and in vivo. The function of CD26 in tumor development is unknown and the machinery with which the CD26 mAb induces its anti-tumor effect remains uncharacterized. Results: The localization of CD26 in the nucleus of T cell leukemia/ lymphoma cells and mesothelioma cells was shown by biochemical and immuno-electron microscopic analysis. The DPPIV enzyme activity was revealed in the nuclear fraction of T cell leukemia/lymphoma cells. These expressions of intra-nuclear CD26 were augmented by treatment with the CD26 mAb, 1F7, with anti-tumor effect against the CD26+ T cell leukemia/lymphoma cells. In contrast, the CD26 mAb, 5F8, without anti-tumor effect, did not augment CD26 expressions in the nucleus. Biotin-labeled, cell surface CD26 translocated into the nucleus constantly, and this translocation was enhanced with 1F7 treatment but not with 5F8. Conclusion: These results indicate that the intra-nuclear CD26 which moves from plasma membrane may play certain roles in cell growth of human cancer cells.
AB - Background: CD26 is a type II, cell surface glycoprotein known as dipeptidyl peptidase (DPP) IV. Previous studies have revealed CD26 expression in T cell leukemia/lymphoma and malignant mesothelioma, and an inhibitory effect of anti-CD26 monoclonal antibody (mAb) against the growth of CD26+ cancer cells in vitro and in vivo. The function of CD26 in tumor development is unknown and the machinery with which the CD26 mAb induces its anti-tumor effect remains uncharacterized. Results: The localization of CD26 in the nucleus of T cell leukemia/ lymphoma cells and mesothelioma cells was shown by biochemical and immuno-electron microscopic analysis. The DPPIV enzyme activity was revealed in the nuclear fraction of T cell leukemia/lymphoma cells. These expressions of intra-nuclear CD26 were augmented by treatment with the CD26 mAb, 1F7, with anti-tumor effect against the CD26+ T cell leukemia/lymphoma cells. In contrast, the CD26 mAb, 5F8, without anti-tumor effect, did not augment CD26 expressions in the nucleus. Biotin-labeled, cell surface CD26 translocated into the nucleus constantly, and this translocation was enhanced with 1F7 treatment but not with 5F8. Conclusion: These results indicate that the intra-nuclear CD26 which moves from plasma membrane may play certain roles in cell growth of human cancer cells.
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U2 - 10.1186/1475-2867-9-17
DO - 10.1186/1475-2867-9-17
M3 - Article
C2 - 19555512
AN - SCOPUS:67651024959
SN - 1475-2867
VL - 9
JO - Cancer Cell International
JF - Cancer Cell International
M1 - 17
ER -
