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Cancer Medication? Potential Tumor Suppressor Identified

Mar. 25, 2009 — The gene Myc is an important factor for the growth of organisms by cell division. It causes the production of a protein which, as a transcription factor, controls the expression of up to 15 % of all human genes. When this gene mutates to an oncogene, the cell proliferates excessively and apoptosis is inhibited. Thereby the gene plays a decisive role in the development of many tumors.


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he problem is that pharmacological substances do not target Myc as it does not have enzymatic activity of its own. Thus, scientists worldwide are trying to find alternative ways to inhibit this oncogene. A team of scientists led by Klaus Bister and Markus Hartl of the Institute of Biochemistry and the Centre for Molecular Biosciences of the University of Innsbruck may have made an important step towards achieving this goal.

Suppressing pathological cell growth

For the first time, the scientists have shown that Myc suppresses the expression of the gene BASP1. This evidence prompted them to test the effect of BASP1 on the oncogene. In cell experiments they proved that BASP1 specifically inhibits the uncontrolled proliferation of Myc. „Until now the precise biochemical function of BASP1 is unknown“, Prof. Bister explains. „However, in our experiments we have found clear evidence that Myc-induced cell transformation can be specifically inhibited by BASP1, and consequently, the gene functions as a tumor suppressor.“ This finding may facilitate the development of new drugs which keep the development of tumors under control.

The scientists are supported by the Austrian Science Fund.

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The above story is reprinted from materials provided by University of Innsbruck, via AlphaGalileo.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


Journal Reference:

  1. Hartl M, Nist A, Khan MI, Valovka T, Bister K. Inhibition of Myc-induced cell transformation by brain acid-soluble protein 1 (BASP1). Proceedings of the National Academy of Sciences, DOI: 10.1073/pnas.0812101106
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