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Carcinogenesis Advance Access originally published online on September 29, 2009
Carcinogenesis 2009 30(11):1872-1879; doi:10.1093/carcin/bgp234
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© The Author 2009. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

The extracellular loop 2 of TM4SF5 inhibits integrin {alpha}2 on hepatocytes under collagen type I environment

Sin-Ae Lee1,2, Young Mee Kim3, Tae Kyoung Kwak1,4, Hyeon Jung Kim1,4, Semi Kim5, Wonil Ko6, Sung-Hoon Kim6, Ki Hun Park7, Hyun Jeong Kim8, Moonjae Cho3 and Jung Weon Lee1,2,4,9,*

1 Cancer Research Institute, College of Medicine, Cell Dynamics Research Center
2 Department of Molecular and Clinical Oncology, Seoul National University, Seoul 110-799, Korea
3 Department of Medicine, Cheju National University, Jeju 690-756, Korea
4 Department of Tumor Biology, Seoul National University, Seoul 110-799, Korea
5 Therapeutic Antibody Research Center, Korea Research Institute of Bioscience and Biotechnology, Taejon 305-333, Korea
6 Cancer Preventive Material Development Research Center, Kyunghee University, Seoul 131-701, Korea
7 Division of Applied Life Science, Environmental Biotechnology National Core Research Center, Gyeongsang National University, Jinju 660-701, Korea
8 Department of Dental Anesthesiology, Seoul National University, Seoul 110-799, Korea
9 Department of Pharmacy, College of Pharmacy, Seoul National University, Seoul 110-799, Korea

* To whom correspondence should be addressed. Tel: +82 2 3668 7030; Fax: +82 2 766 4487; Email: jwl{at}snu.ac.kr

Four-transmembrane L6 family member 5 (TM4SF5) and its homolog L6, a tumor antigen, form a four-transmembrane L6 family. TM4SF5 expression causes uncontrolled cell proliferation and angiogenesis. Although other genuine transmembrane 4 superfamily (TM4SF) members co-operate with integrins for cell migration, roles of TM4SF5 in the cellular spreading and migration are unknown. Using hepatocarcinoma cell clones that ectopically express TM4SF5, we found that cross talks via an extracellular interaction between TM4SF5 and integrin {alpha}2 in collagen type I environment inhibited integrin {alpha}2 functions such as spreading on and migration toward collagen I, which were recovered by suppression of TM4SF5 or structural disturbance of its second extracellular loop using a peptide or mutagenesis. Altogether, the observations suggest that TM4SF5 in hepatocytes negatively regulates integrin {alpha}2 function via an interaction between the extracellular loop 2 of TM4SF5 and integrin {alpha}2 during cell spreading on and migration through collagen I environment.

Abbreviations: ECM, extracellular matrix; shRNA, short hairpin RNA

Received April 4, 2009; revised August 22, 2009; accepted September 19, 2009.


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