'Cell junctions' respond to environmental signals

December 12, 1999

WASHINGTON, D.C. --- Cells have developed a variety of mechanisms for coupling themselves to their neighbors and to their surrounding extracellular world. These so-called 3cell junctions2 are made from many different types of proteins that assemble into structures called gap junctions, tight junctions, adherens junctions, desmosomes and hemidesmosomes, each with a different function.

According to Kathleen Green, professor of pathology at Northwestern University Medical School and a member of The Robert H. Lurie Comprehensive Cancer Center of Northwestern University, it is now clear that intercellular junctions are not simply things that hold cells together but, rather, dynamic structures that respond to environmental signals by breaking and reforming.

In fact, cell junctions are themselves involved in the propagation of signals that control cell growth and motility that contribute to metastasis, the most devastating and life-threatening part of the cancer process.

Green will co-chair a minisymposium on the role of each of these steps in cancer progression at today's meeting of the American Society for Cell Biology. Her co-chair is Margaret Wheelock, of the University of Toledo, Toledo, Ohio. The co-chairs also will present new findings at the symposium.

The symposium will include a description, using the powerful genetic model system Drosophila, of the discovery of a new tumor suppressor gene called scribble, which is a component of intercellular septate junctions. Mutations in tumor suppressor genes lead to uncontrolled cell growth and, consequently, tumor formation. Genes that are first discovered in fruit flies often lead the way to way to important advances in our understanding of human diseases, including cancer.

Another presentation will focus on how a cancer-causing oncogene can alter the communicating function of cellular channels called gap junctions. Others will describe modulation of cadherin-based junctions called adherens junctions and desmosomes, and, for example, how the different properties of cadherins and their associated proteins might dictate whether a breast cancer cell will spread.

The final presentation will be on a new and surprising discovery about how a molecule that tethers cells to extracellular matrix can interact with an actin-binding protein found at cell-cell junctions and even the nucleus, and thus might have unexpected regulatory functions in controlling cell motility.
-end-
(Editor's note: Dr. Green can be reached during the ASCB meeting (Dec. 11-15) at the Grand Hyatt Hotel, Washington, D.C., at 202- 582-1234 and following the meeting at kgreen@nwu.edu )

Northwestern University

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