PITTSBURGH, June 6 -- Mutations in the cell adhesion molecule known as integrin alpha 7 (integrin 7) lead to unchecked tumor cell proliferation and a significantly higher incidence in cancer spread, or metastasis, in several cancer cell lines, report researchers at the University of Pittsburgh School of Medicine in a study being published today in the Journal of the National Cancer Institute. These findings suggest that integrin 7 represents an important new target for cancer therapy and prevention.
Integrin 7 belongs to a major class of cell membrane proteins that play a role in the attachment of a cell to the extracellular matrix (ECM), which is the material that holds cells within a particular type of tissue together. Integrins also help cells attach to one another and are involved in transmitting chemical signals between cells and the ECM.
In this study, the researchers, led by Jianhua Luo, M.D., Ph.D., associate professor in the division of molecular and cellular pathology, University of Pittsburgh School of Medicine, examined whether this gene is mutated in specimens of various human cancers as well as whether the level of integrin 7 expression is associated with clinical relapse of human cancers. They also investigated whether integrin 7 has tumor suppressor activity.
To determine whether mutations in integrin 7 contribute to cancer, Dr. Luo and his collaborators sequenced the integrin 7 genes from 66 human cancer specimens and cell lines representing a number of different kinds of cancer, including cancer of the prostate, liver, brain (glioblastoma) and muscle (leiomyosarcoma).
They found mutations in the integrin 7 gene, particularly those that resulted in an abnormally shortened protein product, or truncation, in 16 of 28 prostate cancers. They also found truncation-inducing mutations in five of 24 liver cancer samples, five of six glioblastomas, and one of four leiomyosarcomas.
Integrin 7 mutations a
Contact: Jim Swyers
University of Pittsburgh Schools of the Health Sciences