Laminin-5 promotes cell motility by regulating the function of the integrin {alpha}6ß1 in pancreatic cancer

Xiaowu Li, Zhengwei Ma, Jin Zhu, Kun Li, Shuguang Wang, Ping Bie and Jiahong Dong

The authors have found that a result reported in the above paper is not reproducible and wish to withdraw it from publication. The paper has been published online in Carcinogenesis Advance Access and the authors hereby retract this paper and discourage citations of it.

For reference, the abstract of the paper is printed below:

Abstract

Laminin-5 and its ligand, the integrin {alpha}6ß1, are associated with the progression of pancreatic cancer. To identify the roles of the integrin {alpha}6ß1 and laminin-5 in regulating the invasive behaviors of pancreatic cancer cells, we analyzed integrin profiles and investigated the mechanisms by which {alpha}6ß1 facilitates laminin-5 deposition in extracellular matrix and by which laminin-5 promotes cell migration via the integrin {alpha}6ß1 in the metastatic pancreatic cancer cell line BxPc3 and the non-metastatic pancreatic cancer cell line PaCa2 using an in vitro cell culture system or a co-culture system of the tumor cells with peritumor fibroblasts (PTF). We found that {alpha}6ß1 was highly expressed in the metastatic pancreatic cancer cell line BxPc3, but poorly expressed in the non-metastatic pancreatic cancer cell line PaCa2. The integrin {alpha}6ß1 not only increased the migration of pancreatic cancer cells, but also facilitated the assembly of laminin-5 into extracellular matrices in the co-cultures of the metastatic pancreatic cancer BxPc3 cells with PTFs. Blocking the function of {alpha}6ß1 with the specific function-blocking antibodies GoH3 suppressed cell migration and the assembly of laminin-5. In addition, laminin-5 promoted cell motility by decreasing the focal adhesions formed by the integrin {alpha}6ß1. These findings suggest that the interaction of laminin-5 with the integrin {alpha}6ß1 plays an important role in promoting the progression of pancreatic cancer.





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