Life, The Universe ...: A New Target for the Treatment of Breast Cancer

The active ingredient in a drug currently being tested to treat rheumatoid arthritis might also one day serve as an effective means of treating one of the deadliest forms of breast cancer.

Researchers with the U.S. Department of Energy’s Lawrence Berkeley National Laboratory have demonstrated that inhibiting the activity of the protease enzyme known as TACE can deprive tumor cells of a key factor needed for their proliferation. TACE is strongly present in a form of breast cancer which responds poorly to current therapies

“We have shown that inhibition of the TACE protease in breast cancer cells blocks the shedding of two critical growth factor proteins and results in an inhibition of a key signaling pathway that controls cell division,” says Paraic Kenny, a post-doctoral cell biologist with the research group of Mina Bissell in Berkeley Lab’s Life Sciences Division. “Based on analysis of cells grown in three-dimensional cultures, the inhibition of this protease results in the reversion of the malignant phenotype of these breast cancer cells and switches their behavior back to a phenotype very reminiscent of non-malignant breast epithelial cells.”

Kenny is the co-author along with Bissell of a paper published in the Journal of Clinical Investigation titled: "Targeting TACE-Dependent EGFR-ligand Shedding in Breast Cancer." This paper presents the latest experimental results from an on-going investigation led by Bissell into the ecology of tumors.

It has long been Bissell’s contention that “no tumor is an island.” Tumor cells, she maintains, exist in the same microenvironment as healthy cells and must therefore appropriate normal physiological processes to facilitate their growth and spread. As she and her colleagues have repeatedly demonstrated, this idea can open up potential new avenues and targets for diagnostic and therapeutic applications.

For this latest paper, Kenny and Bissell looked into the pathway by which the EGFR signal is carried. EGFR, which stands for Epidermal Growth Factor Receptor, is the protein on the outer surface of a cell that is activated by EGF and related growth factors and signals for the cell to divide. Given that one of the hallmarks of cancer is cell division run amok, the reduction of high levels of EGFR activity has long been a primary target for anti-cancer drug development. So far, however, drugs aimed at directly inhibiting EGFR activity have met with only limited success in the cancer clinic, primarily in a small number of lung cancers.

“Because of this, we turned our attention to the processes that regulate the production of the ligands which bind and activate EGFR,” Kenny says. “We reasoned that this binding and activation is essential for EGFR activation and that finding a way to block this interaction might prove to be an important additional approach to explore for inhibition of this pathway.”

Kenny stresses that the importance of EGFR to so many different tumor types, including lung, head and neck, bladder, colorectal and kidney, makes it likely that “TACE inhibition has the potential to be an effective means of stopping tumor growth for EGFR-dependent cancers outside the breast as well.”

<---We all know someone or are some one who has or have had cancer. The most common for women is breast cancer. Slow progress is made in the battle. A new vaccine prevents a virus that causes cervical cancer. Still cancer has no vaccine, nor cure. Scary too is the rise in cases of prostate cancer in men 18-37.--->

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