Tuesday, December 17, 2013

Newly Discovered Regulation of KRas may Result in Novel Cancer Therapies

KRas has been well characterized for its role in several cancers. Mutations of KRas are seen in more than 90% of pancreatic cancer patients, and are prevalent in colon and lung cancer. However, targeting KRas for cancer therapy has been difficult.

Now, an international collaboration of scientists has revealed a new mechanism for regulating KRas function that they hope will provide a new approach for identification of therapeutic targets in cancers with a KRas mutation. Their findings are published in a recent issue of JBC in the article entitled: 'Degradation of Activated K-Ras Orthologue via K-Ras Specific Lysine Residues is Required for Cytokinesis'

This article describes the use of a social ameboid, Dictyostelium, as a powerful model system to study Ras signaling and KRas regulation. They introduced the cancer causing (oncogenic) form of KRas into Dictyostelium, and compared its regulation with normal KRas. They found that these cells recognize the oncogenic KRas and mark it by ubiquitination. Ubiquitination is a process that cells normally use to mark a protein that needs to be recycled, so the ubiquitination of oncogenic KRas leads to it being chopped up and cleared from cells.

The next step is to identify the protein that ubiquitinates oncogenic KRas so that its activity can be increased in cancer cells with mutated KRas.

Some information for this blog was obtained from: Regulation of Cancer-Causing Protein Could Lead to New Therapeutic Targets

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