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Experiments with fruit quality improvement lead to new approach for halting spread of cancer cells

Experimental work aimed at improving the quality of fruit has led to the discovery by Hebrew University of Jerusalem agricultural researchers of a promising new avenue of drug treatment for halting the growth and spread of cancer cells in animals and humans.

Their approach has been shown to inhibit the malignant cells without affecting normal cells and without the severe side effects of traditional treatments such as radiation and chemotherapy. The strategy involves isolating the malignant tumor from its nutritional and oxygen supplies, thereby halting its growth and stopping metastases (spread of cancer cells to other parts of the body).

The work on the project was carried out at the Hebrew University Faculty of Agricultural, Food and Environmental Quality Sciences in Rehovot by Prof. Oded Shoseyov, Dr. Levava Roiz, Dr. Patricia Smirnoff and Dr. Betty Schwartz. Their discoveries were published recently in the journal Cancer of the American Cancer Society.

The approach of the Hebrew University researchers is based on the actions of actibind, a protein that is produced by the black mold Aspergillus niger and that is a well-known microorganism used in bio and food technology. In plants, actibind binds actin, a major component of the intracellular structure in plants, interfering with the plants' pollen tubes and halting cell growth.

While the Hebrew University researchers were initially interested in the activity of actibind in connection with a horticultural project aimed at improving the quality of peaches and nectarines, an actibind-like protein, RNaseT2, was also subsequently found to bind actin in human and animal migrating cells, such as the cells that are responsible for new blood vessel formation (angiogenesis) in tumors.

By blocking the blood supply to the tumors, actibind halted the ability of malignant cells to move through the blood stream to form new metastases. A further plus is that actibind is not toxic to normal cells, thereby significantly minimizing the risk of side effects.

In laboratory experiments using cell cultures that originated from human colon cancer, breast cancer and melanoma, increasing the level of actibind was found to reduce the ability of these cells to form tumorogenic colonies. Further experimentation, with a variety of animal models, showed that the increased actibind inhibited the growth of colon cancer-derived tumors, metastases and blood vessel formation. These promising discoveries were detailed in the Cancer article.

The results shown in working with actibind led to a further development in the researchers' project. During the completion of the human genome project, the gene encoding for RNaseT2, the human actibind-like protein, was found on chromosome 6. The Hebrew University team used genetic engineering procedures to produce a recombinant RNaseT2 protein that showed an impressive anti-cancer potential. These results have raised broad interest in international scientific meetings and in business circles.

The fungal actibind and the human RNaseT2 represent the basis for a new class of drugs that could be used as a front-line therapy in the fight against cancer, say the researchers.

Jerry Barach | EurekAlert!
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